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Pojačava li simpatički živčani sustav ili smanjuje mokrenje?

Pojačava li simpatički živčani sustav ili smanjuje mokrenje?



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prema mojoj knjizi:

Stimulacija simpatičkog živčanog sustava, dovodi do oslobađanja noradrenalina (noradrenalina), pripremajući tijelo za odgovor "Bori se ili bježi".

Također se navodi da:

Učinak simpatičke stimulacije je održavanje urinarne kontinencije.

Ali ako stimulacija simpatikusa rezultira kontinencijom mokraće, zašto više mokrimo kad smo u strahu ili nervozni?


Pročitao sam ovo pitanje, ali prihvaćeni odgovor kaže da se adernalin (epinefrin) oslobađa (ne norepinefrin) i ne pruža dokaze koji potkrepljuju zašto adernalin dovodi do pojačanog mokrenja.


Koja je uloga simpatičkog živčanog sustava u neuroanatomiji neurogenog mjehura?

Kada je simpatički živčani sustav aktivan, uzrokuje povećanje kapaciteta mokraćnog mjehura bez povećanja pritiska detruzora u mirovanju (akomodacije) i stimulira unutarnji urinarni sfinkter da ostane čvrsto zatvoren. Djelovanje simpatikusa također inhibira parasimpatičku stimulaciju, sprječavajući kontrakcije mokraćnog mjehura. Kada je simpatički živčani sustav aktivan, dolazi do akomodacije mokraće i potisnut je refleks mokrenja.

Povezana pitanja:

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Tablice

Informacije o suradnicima i otkrivanja

Bradley C Gill, MD, MS Glavni specijalizant, Odjel za urologiju, Klinički instruktor kirurgije Instituta za urologiju i bubrege Glickman, Cleveland Clinic Lerner College of Medicine, Konzultantsko osoblje Instituta za obrazovanje, Odjel za biomedicinsko inženjerstvo, Lerner Research Institute, Cleveland Clinic

Objavljivanje: Ništa za otkriti.

Sandip P Vasavada, dr.med Izvanredni profesor kirurgije, Cleveland Clinic Lerner College of Medicine Physician, Centar za žensku urologiju i genitourinarnu rekonstruktivnu kirurgiju, The Glickman Urološki i bubrežni institut Zajednički sastanak s Institutom za žene, Cleveland Clinic

Otkrivanje: Služiti(d) kao direktor, službenik, partner, zaposlenik, savjetnik, konzultant ili povjerenik za: Medtronic, Axonics, BlueWind<br/>Primio vlasnički interes od NDI Medical, LLC za članstvo u panelu za reviziju Primio konzultantsku naknadu od allergana za govor i podučavanje Primljena konzultantska naknada od medtronic-a za govor i podučavanje Primljena konzultantska naknada od bostonskog znanstvenog savjetovanja. za: Oasis Consumer Healthcare.

Farzeen Firoozi, dr.med Klinička suradnica, Centar za žensku urologiju i rekonstruktivnu kirurgiju zdjelice, Glickman Urološki institut, Cleveland Clinic Foundation

Farzeen Firoozi, MD član je sljedećih medicinskih društava: American Medical Association, American Urological Association

Objavljivanje: Ništa za otkriti.

Raymond R Rackley, dr.med Profesor kirurgije, Cleveland Clinic, Lerner College of Medicine, Medicinski liječnik, Centar za neurourologiju, Zdravlje ženske zdjelice i Rekonstruktivnu kirurgiju žena, Glickman Urološki institut, Cleveland Clinic, Beachwood Family Health Center, i Willoughby Hills Family Health Center direktor, The Urothel Bi, direktorica The Laboratory Bi Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD član je sljedećih medicinskih društava: American Urological Association

Objavljivanje: Ništa za otkriti.

Francisco Talavera, dr. sc Dodatni docent, Sveučilište Nebraska Medical Center College of Pharmacy, glavni urednik, Medscape Drug Reference

Otkrivanje: Primio plaću od Medscapea za zaposlenje. za: Medscape.

Edward David Kim, MD, FACS Profesor kirurgije, Odsjek za urologiju, Konzultantsko osoblje Medicinskog fakulteta Sveučilišta Tennessee, Medicinski centar Sveučilišta Tennessee

Otkrivanje: Služiti(d) kao govornik ili član biroa za govornike za: Endo.

Raymond R Rackley, dr.med Profesor kirurgije, Cleveland Clinic, Lerner College of Medicine, Medicinski liječnik, Centar za neurourologiju, Zdravlje ženske zdjelice i Rekonstruktivnu kirurgiju žena, Glickman Urološki institut, Cleveland Clinic, Beachwood Family Health Center, i Willoughby Hills Family Health Center direktor, The Urothel Bi, direktorica The Laboratory Bi Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD član je sljedećih medicinskih društava: American Urological Association

Objavljivanje: Ništa za otkriti.

Šlomo Raz, dr.med Profesor, Odjel za kirurgiju, Odjel za urologiju, Sveučilište Kalifornije, Los Angeles, Medicinski fakultet David Geffen

Objavljivanje: Ništa za otkriti.

Michael S Ingber, dr.med Klinički suradnik, Glickman Urološki i bubrežni institut klinike Cleveland


Sve što trebate znati o simpatičkom živčanom sustavu

Kako vaše tijelo reagira na stresne situacije? Jeste li se ikada zapitali zašto vam srce odjednom ubrzano kuca i oblije vas znoj kada naiđete na neki oblik opasnosti? To je gotovo automatski odgovor koji se javlja kad god osjetite prijetnju, bilo da se radi samo o potencijalnoj neugodnoj situaciji ili stvarno zastrašujućoj situaciji kao što je napad stranca. Ovu reakciju bori se ili bježi donosi vaš simpatički živčani sustav, koji vam obično pomaže nositi se sa stresom.

Što je simpatički živčani sustav?

Dok vaš mozak, koji je vitalni dio središnjeg živčanog sustava, ima sposobnost kontrolirati vaše svjesne radnje poput hodanja, razmišljanja i govora, vaše tijelo također ima autonomni živčani sustav, koji regulira vaše tjelesne funkcije, poput otkucaja vašeg srce, vaše disanje, način na koji probavljate hranu, obrasci znojenja itd.

Autonomni sustav ima dva odjela. Sastoji se od simpatičkog i parasimpatičkog živčanog sustava. Primarna funkcija simpatičkog sustava je stimulirati vaše odgovor bori se ili bježi, što je fiziološka reakcija koja se događa kao odgovor na percipirani štetni događaj, napad ili prijetnju opstanku. Parasimpatički sustav omogućuje vam održavanje normalnih funkcija kao što su probava i održavanje tijela u mirovanju.

Struktura simpatičkog živčanog sustava

Prijenos signala u sustavu ostvaruje se kroz mrežu živčanih stanica zvanih neuroni. Postoje dvije vrste neurona: preganglijski neuroni i postganglijski neuroni. Preganglijski neuroni imaju kratka vlakna koja potječu iz torakolumbalnih segmenata leđne moždine, koja komuniciraju s ganglijama uz kralježnični stup, a sinapse s dužim postganglijskim neuronima.

Preganglijski neuroni sinapsiraju s ganglijama i oslobađaju kemikaliju (neurotransmiter) nazvanu acetilkolin, koja aktivira receptore na postganglijskim neuronima. Postganglijski neuroni zauzvrat otpuštaju hormon zvan norepinefrin, koji cilja adrenergičke receptore na različitim organima i tkivima. Stimulacija ovih ciljnih receptora rezultira karakterističnim odgovorima bori se ili bježi.

Postoje dvije iznimke od gore navedenih procesa, a to su postganglijski neuroni koji se nalaze u žlijezdama znojnicama i kromafinske stanice koje se nalaze u meduli nadbubrežne žlijezde. Postganglijski neuroni ispuštaju acetilkolin kako bi aktivirali muskarinske receptore, osim na dlanovima, tabanima i drugim područjima s debelom kožom. U tim područjima norepinefrin djeluje na adrenergičke receptore. Kromafinske stanice koje se nalaze u nadbubrežnoj meduli su ekvivalentne postganglijskim neuronima. Preganglijski neuroni komuniciraju s kromafinskim stanicama i potiču ih da otpuštaju epinefrin i norepinefrin izravno u krv.

Dva hormona iza aktivacije simpatikusa

Simpatički živčani sustav oslobađa dva hormona unutar tijela kao odgovor na stres, što rezultira "naletom adrenalina" ili osjećajem hitnosti koji se javlja tijekom stresnih stanja. Ti se hormoni zovu epinefrin i norepinefrin, koji pomažu vašem tijelu da radi optimalno tijekom takvih događaja.

Nakon aktivacije vašeg sustava, norepinefrin se oslobađa kako bi pripremio tijelo za početne faze stresa. Ako se stres brzo riješi, tjelesne funkcije se vraćaju u normalu. Međutim, ako stresni događaj potraje, vaše tijelo proizvodi epinefrin kako bi pojačao te učinke i aktivirao različite dijelove tijela da reagiraju u skladu s tim.

Što se događa ako se aktivira simpatički živčani sustav?

Kada se netko suoči s opasnom ili stresnom situacijom, simpatički se živčani sustav automatski aktivira bez svjesne kontrole. Gotovo istovremeno se aktiviraju različite tjelesne funkcije kao što su:

  1. Poticanje nadbubrežnih žlijezda na oslobađanje norepinefrina i epinefrina, koji su odgovorni za niz reakcija povezanih sa stresom.
  2. Povećanje broja otkucaja srca, što rezultira povećanom isporukom kisika i hranjivih tvari u mozak i mišiće kako bi ih pripremili za stres.
  3. Povećanje glukoze koja se oslobađa iz jetre u krvotok kako bi se mišićima pružila više energije.
  4. Širenje dišnih puteva (bronhiola) u plućima kako bi se omogućilo više zraka, što povećava opskrbu kisikom krvi i ostatka tijela.
  5. Dilatacija zjenica, koja se često opaža kada ste iznenađeni ili vam prijete.
  6. Usporavanje probavne aktivnosti, što pomaže u očuvanju energije vašeg tijela koja se može koristiti za obranu od stresa.
  7. Opuštanje mokraćnog mjehura, što vam omogućuje da zadržite urin dok ste pod stresom. Međutim, u pogoršanim situacijama, neki ljudi nehotice gube kontrolu nad mjehurom zbog straha koji im dopušta da ih tijelo pusti.

Ovo su samo neke od uobičajenih funkcija uključenih u reakciju bori se ili bježi koju regulira vaš simpatički živčani sustav. Zbog ovakvih tjelesnih reakcija vaše tijelo je spremno za trčanje, borbu, podizanje utega ili reagiranje prema potrebi, ovisno o konkretnim prijetećim situacijama. Kada se situacija razriješi, funkcije simpatikusa se vraćaju u stanje mirovanja, omogućujući vam da se vaš otkucaj srca vrati u normalu, da se vaše disanje uspori, a druge funkcije tijela da se vrate u uravnoteženo stanje.


Razlike između simpatičkog i parasimpatičkog živčanog sustava

Simpatički i parasimpatički sustav dio su perifernog živčanog sustava. Ovdje objašnjavamo razlike među njima.

Simpatički i parasimpatički sustav dio su perifernog živčanog sustava. Ovdje objašnjavamo razlike među njima.

Simpatički i parasimpatički sustav zajedno su dio živčanog sustava. Djeluju u tandemu kako bi održali stanje homeostaze u tijelu. Prije nego što nastavimo s razumijevanjem različitih odgovora i učinaka ova dva sustava, moramo razumjeti odakle ta dva sustava potječu.

Živčani sustav dijeli se na središnji živčani sustav (koji se sastoji od mozga i leđne moždine) i periferni živčani sustav (koji se sastoji od živčanih grana koje proizlaze iz mozga i leđne moždine). Periferni živčani sustav se dalje dijeli na somatski i autonomni sustav. To je autonomni živčani sustav koji se dijeli na simpatički i parasimpatički živčani sustav.

Simpatički živčani sustav

Želite li nam pisati? Pa, tražimo dobre pisce koji žele širiti vijest. Javite nam se pa ćemo razgovarati.

Simpatički živčani sustav je jedan od dijelova perifernog živčanog sustava. Simpatički živci potječu od kralježnjaka počevši od prvog torakalnog segmenta leđne moždine, protežući se prema gore do drugog ili trećeg lumbalnog segmenta. Glavna funkcija simpatičkog živčanog sustava je mobilizirati odgovor tijela u stresnim okolnostima. Dakle, simpatički živčani sustav inicijalizira odgovor tijela ‘borba ili bijeg’. Simpatički sustav inervira mnoge različite organe u tijelu, kao što su oči, pluća, bubrezi, gastrointestinalni trakt, srce, itd. Uzrokuje povećanje broja otkucaja srca i brzine izlučivanja. Također povećava lučenje renina iz bubrega. Također postoji stimulacija oslobađanja glukoze iz jetre, koja se oslobađa u krv, kako bi bila dostupna tijelu.

Parasimpatički živčani sustav

Parasimpatički živčani sustav je dio autonomnog živčanog sustava. Ovo je dio autonomnog živčanog sustava koji je odgovoran za fazu ‘odmora i probave’ u tijelu. Živci ovog sustava šalju vlakna u srčane mišiće, glatke mišiće i žljezdano tkivo. Parasimpatički živčani sustav odgovoran je za povećanje lučenja sline, proizvodnju suza, mokrenje, probavu i defekaciju. Osnovni parasimpatički sustav uključuje funkcije i radnje koje ne zahtijevaju trenutnu reakciju u okruženju.

Razlika između simpatičkog i parasimpatičkog sustava

Postoje mnoge razlike koje postoje, jer ova dva sustava djeluju na suprotan način.

Parasimpatički živčani sustav: Suženje zjenica
Simpatički živčani sustav: Proširenje zjenica

Parasimpatički živčani sustav: Poticanje lučenja sline
Simpatički živčani sustav: Inhibicija lučenja sline

Parasimpatički živčani sustav: Smanjuje broj otkucaja srca, što uzrokuje pad krvnog tlaka
Simpatički živčani sustav: Povećava broj otkucaja srca, što uzrokuje povećanje krvnog tlaka

Parasimpatički živčani sustav: Sužava bronhije, čime se smanjuje promjer dišnih puteva
Simpatički živčani sustav: Proširuje bronhije, čime se povećava promjer dišnih puteva

Parasimpatički živčani sustav: Potiče aktivnost probavnog sustava, poput stimulacije peristaltike
Simpatički živčani sustav: Inhibira aktivnost probavnog sustava, poput inhibicije peristaltike

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Parasimpatički živčani sustav: Potiče izlučivanje žučnog mjehura
Simpatički živčani sustav: Smanjuje izlučivanje žučnog mjehura

Parasimpatički živčani sustav: Skuplja mokraćni mjehur
Simpatički živčani sustav: Opušta mokraćni mjehur

Parasimpatički živčani sustav: Opušta rektum
Simpatički živčani sustav: Ugovori rektum

Dakle, kao što se može zaključiti iz gore navedene tablice, odgovori i učinci oba sustava su komplementarni po prirodi, a ne antagonistički. Simpatički odjel djeluje kao akcelerator, a parasimpatički odjel djeluje kao usporavač ljudskog tijela. Dakle, ova dva sustava pokušavaju održati tijelo u normalnom stanju homeostaze maksimalno moguće vrijeme. Istovremeno se u tijelu aktivira samo jedan od dvaju sustava ovisno o vrsti inervacije koja je nastala i hormonima koji se oslobađaju.


Simpatički živčani sustav i regulacija volumena krvi: lekcije pacijenata s autonomnim zatajenjem

Bolesnici s autonomnim zatajenjem pružaju jedinstvenu priliku za proučavanje uloge simpatičke funkcije u regulaciji volumena krvi. Ovi pacijenti imaju preokret u odnosu na normalne dnevne varijacije u izlučivanju mokraće i imaju dvostruko veću natriurezu tijekom noći. Pacijenti s autonomnim zatajenjem također nisu u stanju sačuvati natrij i ne uspijevaju smanjiti natriurezu kao odgovor na ograničenje natrija u prehrani. Dok normalni subjekti mogu održavati krvni tlak unutar uskih vrijednosti u širokom rasponu volumena plazme, krvni tlak je linearno povezan s promjenama volumena plazme u pacijenata s autonomnim zatajenjem. Fludrokortizon se često koristi za povećanje volumena plazme u ovih bolesnika, ali je taj učinak samo prolazan, a njegova dugoročna učinkovitost vjerojatno je posljedica potenciranja presorskih učinaka norepinefrina. S druge strane, epoetin-alfa je učinkovit u ispravljanju blage anemije koju pacijenti s autonomnim zatajenjem obično imaju i poboljšava njihovu ortostatsku hipotenziju dijelom povećanjem intravaskularnog volumena. Pacijenti s autonomnim zatajenjem, stoga, ilustriraju ulogu simpatičkog živčanog sustava u regulaciji natrija i volumena. Suprotno tome, dijeta s visokim udjelom soli izaziva inhibiciju simpatikusa u normalnih ispitanika. Paradoksalno, simpatička aktivnost je povećana u bolesnika s hipertenzijom osjetljivom na sol i doprinosi njihovom porastu krvnog tlaka. Stoga su u oba ova stanja narušeni mehanizmi povratne sprege koji uključuju simpatički živčani sustav i homeostazu volumena.


Središnji mehanizmi koji reguliraju NSRS

Razina RSNA ovisi o neuronskoj aktivnosti u simpatičkim premotornim jezgrama u moždanom deblu i hipotalamusu, uključujući rostralnu ventrolateralnu i ventromedijalnu medulu [rostralnu ventrolateralnu medulu (RVLM), RVMM] i paraventrikularnu jezgru (PVN). RVLM je simpato-ekscitatoran i igra ključnu ulogu u regulaciji aktivnosti eferentnog bubrežnog živca. Neuroni u RVLM projektiraju na preganglijske neurone u intermedijolateralnom staničnom stupcu leđne moždine, koji preko postganglijski neuroni, projektiraju na periferne organe kao što su srce, arterije i bubrezi (19). Značajno smanjenje krvnog tlaka nakon destrukcije premotornih neurona u RVLM-u dokaz je njegove važne uloge (20). Aktivnost premotornih neurona u RVLM i PVN modulirana je bubrežnim mehanizmom i kemoreceptorskim refleksima posredovanim preko bubrežni aferentni živci (4). Središnji i periferni mehanizmi simpatičke regulacije bubrega sažeti su na slici 2 (19).

Slika 2. Shematski dijagram središnjih i perifernih mehanizama simpatičke regulacije srca, krvnih žila i bubrega. RVLM igra ključnu ulogu kao kardiovaskularni centar koji prima i integrira periferne signale dajući informacije o krvnom tlaku, volumenu tekućine i zasićenosti kisikom. Trenutne promjene krvnog tlaka percipiraju baroreceptori i prenose u NTS kao ulazni signal barorefleksne kontrole simpatičkog odljeva. Stimulacija SFO cirkulirajućim angiotenzinom II povećava eferentnu simpatičku aktivnost kroz aktivaciju PVN i RVLM neurona. Inhibicijski putevi se aktiviraju između lamina terminalis i PVN kao odgovor na natrij u plazmi. Povećana aktivnost RVLM neurona prenosi se na intermedijolateralni stanični stup leđne moždine, gdje se aktiviraju periferni simpatički živci srca, arterija i bubrega. RVLM, rostralna ventrolateralna medula NTS, nucleus tractus solitarius CVLM, kaudalna ventrolateralna moždina PVN, paraventrikularna jezgra SFO, subfornični organ.

Kao odgovor na povećanje krvnog tlaka, aktivacija karotidnog sinusa i depresornih živaca aorte stimulira neurone u nucleus tractus solitarius (NTS), koji projiciraju i aktiviraju neurone u kaudalnoj ventrolateralnoj meduli (CVLM). Neurotransmisija između CVLM i RVLM posredovana je inhibicijskim GABAergijskim neuronima, koji potiskuju neuronsku aktivnost u RVLM, smanjuju aktivnost simpatičkog živca, a time i krvni tlak (19). Bubrežni aferentni osjetni živci projiciraju na RVLM preko NTS i PVN, gdje postoji integracija aferentnih signala iz bubrega, izazvanih događajima kao što su ishemija, oksidativni stres i promijenjene razine angiotenzina II i glukoze. Važnost bubrežnih aferentnih refleksa dokazana je nalazom da je povećanje lučenja norepinefrina iz hipotalamusa uzrokovano ozljedom bubrega (21) ukinuto aferentnom bubrežnom denervacijom u štakora (22).

U mozgu postoje brojni neurotransmiteri koji moduliraju aktivnost simpatičkih živaca, jedan od njih je dušikov oksid (NO) koji djeluje i kao neurotransmiter i kao neuromodulator (23). Čini se da endogena proizvodnja NO, inducirana neuronskom NO sintazom (NOS) i inducibilnom NOS, ima različite učinke na krvni tlak i aktivnost simpatičkog živčanog sustava (24, 25). Smatralo se da se to barem djelomično može pripisati različitoj količini oslobođenog neurotransmitera, naime simpato-ekscitatornog l-glutamata i inhibitornog GABA unutar RVLM-a (25). Mikroinjekcija egzogenog NO sugerira cikličke 3′-5′ mehanizme ovisne o gvanozin monofosfatu u modulaciji neuronske aktivnosti (26).

Učinci aktivacije NO sustava unutar središnjeg simpatičkog živčanog sustava također su posredovani supresijom oslobađanja angiotenzina II. Budući da je središnji angiotenzin II povišen i stimulira stvaranje superoksidnih radikala u kardiovaskularnim bolestima, NO posredovana modulacija simpatičkog živčanog sustava ozbiljno je poremećena u ispitanika s hipertenzijom ili zatajenjem bubrega u završnoj fazi (25, 27). U štakora Wistar Kyoto (WKY), prekomjerna ekspresija inducibilnog NOS u RVLM-u navodno je povećala krvni tlak, koji je bio povezan s prekomjernom aktivnošću simpatikusa i bio je oslabljen antioksidativnim tempolom (24). Inhibicija neuronskog oksidativnog stresa može stoga predstavljati učinkovit pristup smanjenju neurohumoralne aktivacije kod kardiovaskularnih bolesti i zatajenja bubrega.


Kakvi su učinci na bol?

Pokazalo se da je živčani sustav, točnije simpatički živčani sustav, vrlo osjetljiv na društvene utjecaje i stres. To objašnjava zašto ako imate stresan tjedan na poslu ili se voljena osoba ne osjeća dobro, možda ćete primijetiti da bol koju možda osjećate postaje gora od uobičajene. U nekim slučajevima također možete shvatiti da je početak vaših bolnih iskustava započeo u vrijeme kada se u vašem životu događalo mnogo stresnih događaja koji sugeriraju da je bol možda više proizvod živčanog sustava, a ne fizičke ozljede.

Više od normalne razine cirkulirajućeg adrenalina s vremenom može povećati našu osjetljivost na bolne podražaje i ponekad biti odgovorno za stvaranje boli samo po sebi. U ovom 'namotanom' stanju bolni osjećaji mogu postati bolniji, a osjećaji koji inače nisu bolni mogu postati jako bolni.

Na primjer, četkanje ruke s ručnika da osušite ruke može uzrokovati bol. To onda uzrokuje da postanete više zabrinuti, što zauzvrat više pokreće živčani sustav i ulazite u začarani krug: živčani sustav završava što dovodi do više boli što može rezultirati većom brigom, stresom i lošijim spavanjem koji uzrokuje više napuštanja a onda daljnja bol.

Kada osjetite bol bilo gdje u tijelu, senzorni centri mozga tada se počinju prilagođavati i mijenjati što rezultira nečim što su neki stručnjaci nazvali 'pamćenjem boli'. Što je vaša bol trajnija i što je duže traje, to je veće područje zahvaćeno u mozgu. Ako se ovaj proces, koji se naziva središnja senzibilizacija, javlja više od 3 mjeseca, bol se može nazvati trajnom ili kroničnom.


Simpatički i parasimpatički živčani sustav dio su Autonomni živčani sustav, koji je ogranak PERIFERNI ŽIVČANI SUSTAV. Druga grana perifernog živčanog sustava je somatski živčani sustav. Periferni živčani sustav proizlazi iz središnjeg živčanog sustava, koji uključuje mozak i leđnu moždinu.

Koja je razlika između autonomnog i somatskog živčanog sustava budući da su oba dio perifernog živčanog sustava? Autonomni sustav (simpatički i parasimpatički) kontrolira nevoljne funkcije naših unutarnjih organa i žlijezda. Na primjer, simpatički živčani sustav pomaže našem tijelu da se nosi sa stresom i poznat je kao "bori se ili bježi" sustav. Dok parasimpatikus uravnotežuje naš sustav kada se stresor ukloni i omogućuje našem tijelu da se odmori. Ovaj sustav je poznat kao “odmori se i probaj” sustav.

Nasuprot tome, somatski sustav kontrolira dobrovoljne funkcije našeg tijela. Na primjer, ako dodirnete nešto vruće, vaš središnji živčani sustav obrađuje te informacije i šalje ih vašem perifernom živčanom sustavu, što uzrokuje da vaš somatski sustav odmah makne vašu ruku s vrućeg predmeta.

The autonomni sustav je jedinstven jer ima DVA neurona koja sinapse (sastaju) u autonomnom gangliju. To je važno jer svaki sustav (simpatički i parasimpatički) ima preganglijske i postganglijske neurone, koji se sastoje od posebnih vlakana (poput kolinergičkih, adrenergičkih itd.) i to određuje koji će se tip neurotransmitera osloboditi.


Sve što trebate znati o vagusnom živcu

Vagusni živac je najduži i najsloženiji od 12 pari kranijalnih živaca koji izlaze iz mozga. On prenosi informacije na ili s površine mozga u tkiva i organe na drugim mjestima u tijelu.

Naziv "vagus" dolazi od latinskog izraza za "lutanje". To je zato što vagusni živac luta iz mozga u organe u vratu, prsima i trbuhu.

Također je poznat kao 10. kranijalni živac ili kranijalni živac X.

Podijeli na Pinterestu Živac vagus jedan je od kranijalnih živaca koji povezuje mozak s tijelom.

Vagusni živac ima dva snopa tijela osjetnih živčanih stanica i povezuje moždano deblo s tijelom. It allows the brain to monitor and receive information about several of the body’s different functions.

There are multiple nervous system functions provided by the vagus nerve and its related parts. The vagus nerve functions contribute to the autonomic nervous system, which consists of the parasympathetic and sympathetic parts.

The nerve is responsible for certain sensory activities and motor information for movement within the body.

Essentially, it is part of a circuit that links the neck, heart, lungs, and the abdomen to the brain.

What does the vagus nerve affect?

The vagus nerve has a number of different functions. The four key functions of the vagus nerve are:

  • Osjetna: From the throat, heart, lungs, and abdomen.
  • Special sensory: Provides taste sensation behind the tongue.
  • Motor: Provides movement functions for the muscles in the neck responsible for swallowing and speech.
  • Parasimpatikus: Responsible for the digestive tract, respiration, and heart rate functioning.

Its functions can be broken down even further into seven categories. One of these is balancing the nervous system.

The nervous system can be divided into two areas: sympathetic and parasympathetic. The sympathetic side increases alertness, energy, blood pressure, heart rate, and breathing rate.

The parasympathetic side, which the vagus nerve is heavily involved in, decreases alertness, blood pressure, and heart rate, and helps with calmness, relaxation, and digestion. As a result, the vagus nerve also helps with defecation, urination, and sexual arousal.

Other vagus nerve effects include:

  • Communication between the brain and the gut: The vagus nerve delivers information from the gut to the brain.
  • Relaxation with deep breathing: The vagus nerve communicates with the diaphragm. With deep breaths, a person feels more relaxed.
  • Decreasing inflammation: The vagus nerve sends an anti-inflammatory signal to other parts of the body.
  • Lowering the heart rate and blood pressure: If the vagus nerve is overactive, it can lead to the heart being unable to pump enough blood around the body. In some cases, excessive vagus nerve activity can cause loss of consciousness and organ damage.
  • Fear management: The vagus nerve sends information from the gut to the brain, which is linked to dealing with stress, anxiety, and fear – hence the saying, “gut feeling.” These signals help a person to recover from stressful and scary situations.

Stimulation of the vagus nerve is a medical procedure that is used to try to treat a variety of conditions. It can be done either manually or through electrical pulses.

The effectiveness of vagus nerve stimulation has been tested through clinical trials. Consequently, the United States Food and Drug Administration (FDA) has approved its use to treat two different conditions.

Epilepsy

In 1997, the FDA allowed the use of vagus nerve stimulation for refractory epilepsy.

This involves a small, electrical device, similar to a pacemaker, being placed in a person’s chest. A thin wire known as a lead runs from the device to the vagus nerve.

The device is placed in the body by surgery under general anesthetic. It then sends electrical impulses at regular intervals, throughout the day, to the brain via the vagus nerve to reduce the severity, or even stop, seizures.

Side effects of vagus nerve stimulation for epilepsy include:

  • hoarseness or changes in voice
  • otežano disanje
  • kašalj
  • slow heart rate
  • difficulty swallowing
  • stomach discomfort or nausea

People using this form of treatment should always tell their doctor if they are having any problems as there may be ways to reduce or stop these.

Mental illness

In 2005, the FDA approved the use of vagus nerve stimulation as a treatment for depression. It has also been found to help with the following conditions:


37.3 Regulation of Body Processes

Hormoni imaju širok raspon učinaka i moduliraju mnoge različite tjelesne procese. Ključni regulatorni procesi koji će se ovdje ispitati su oni koji utječu na sustav izlučivanja, reproduktivni sustav, metabolizam, koncentraciju kalcija u krvi, rast i odgovor na stres.

Hormonal Regulation of the Excretory System

Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The pituitary gland has two components: anterior and posterior. The anterior pituitary is composed of glandular cells that secrete protein hormones. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.

The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH) , which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above 300 mOsm/L, which in turn, raises ADH secretion and water will be retained, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys. Once at the kidneys, ADH changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus, and ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.

Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus . If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.

Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone , a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na + reabsorption and K + secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na + and K + , aldosterone is referred to as a mineralocorticoid , a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na + from sweat, saliva, and gastric juice. The reabsorption of Na + also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.

Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release, as illustrated in Figure 37.7. When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin . Renin, an enzyme, circulates in the blood and reacts with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone and then causes the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na + reabsorption, water retention, and an increase in blood pressure. Angiotensin II in addition to being a potent vasoconstrictor also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.

Hormonal Regulation of the Reproductive System

Regulation of the reproductive system is a process that requires the action of hormones from the pituitary gland, the adrenal cortex, and the gonads. During puberty in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testes in males and ovaries in females) and therefore are called gonadotropins . In both males and females, FSH stimulates gamete production and LH stimulates production of hormones by the gonads. An increase in gonad hormone levels inhibits GnRH production through a negative feedback loop.

Regulation of the Male Reproductive System

In males, FSH stimulates the maturation of sperm cells. FSH production is inhibited by the hormone inhibin, which is released by the testes. LH stimulates production of the sex hormones ( androgens ) by the interstitial cells of the testes and therefore is also called interstitial cell-stimulating hormone.

The most widely known androgen in males is testosterone. Testosterone promotes the production of sperm and masculine characteristics. The adrenal cortex also produces small amounts of testosterone precursor, although the role of this additional hormone production is not fully understood.

Svakodnevna veza

The Dangers of Synthetic Hormones

Some athletes attempt to boost their performance by using artificial hormones that enhance muscle performance. Anabolic steroids, a form of the male sex hormone testosterone, are one of the most widely known performance-enhancing drugs. Steroids are used to help build muscle mass. Other hormones that are used to enhance athletic performance include erythropoietin, which triggers the production of red blood cells, and human growth hormone, which can help in building muscle mass. Most performance enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, the Major League Baseball, and the National Football League.

The side effects of synthetic hormones are often significant and non-reversible, and in some cases, fatal. Androgens produce several complications such as liver dysfunctions and liver tumors, prostate gland enlargement, difficulty urinating, premature closure of epiphyseal cartilages, testicular atrophy, infertility, and immune system depression. The physiological strain caused by these substances is often greater than what the body can handle, leading to unpredictable and dangerous effects and linking their use to heart attacks, strokes, and impaired cardiac function.

Regulation of the Female Reproductive System

In females, FSH stimulates development of egg cells, called ova, which develop in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries, as illustrated in Figure 37.9. Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle.

In addition to producing FSH and LH, the anterior portion of the pituitary gland also produces the hormone prolactin (PRL) in females. Prolaktin stimulira proizvodnju mlijeka u mliječnim žlijezdama nakon poroda. Prolactin levels are regulated by the hypothalamic hormones prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) , which is now known to be dopamine. PRH potiče oslobađanje prolaktina, a PIH ga inhibira.

The posterior pituitary releases the hormone oxytocin , which stimulates uterine contractions during childbirth. Glatki mišići maternice nisu jako osjetljivi na oksitocin sve do kasne trudnoće kada broj receptora za oksitocin u maternici dostiže vrhunac. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. As these cells contract, milk is forced from the secretory alveoli into milk ducts and is ejected from the breasts in milk ejection (“let-down”) reflex. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.

Hormonal Regulation of Metabolism

Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels. Additional regulation is mediated by the thyroid hormones.

Regulation of Blood Glucose Levels by Insulin and Glucagon

Cells of the body require nutrients in order to function, and these nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. Insulin also increases glucose transport into certain cells, such as muscle cells and the liver. This results from an insulin-mediated increase in the number of glucose transporter proteins in cell membranes, which remove glucose from circulation by facilitated diffusion. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. However, this does not occur in all cells: some cells, including those in the kidneys and brain, can access glucose without the use of insulin. Insulin also stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins. These actions mediated by insulin cause blood glucose concentrations to fall, called a hypoglycemic “low sugar” effect, which inhibits further insulin release from beta cells through a negative feedback loop.

This animation describe the role of insulin and the pancreas in diabetes.

Impaired insulin function can lead to a condition called diabetes mellitus , the main symptoms of which are illustrated in Figure 37.10. This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis . Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis . Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure 37.11.

Vizualna veza

Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true?

  1. A pancreatic tumor and type I diabetes will have the opposite effects on blood sugar levels.
  2. A pancreatic tumor and type I diabetes will both cause hyperglycemia.
  3. A pancreatic tumor and type I diabetes will both cause hypoglycemia.
  4. Both pancreatic tumors and type I diabetes result in the inability of cells to take up glucose.

Regulation of Blood Glucose Levels by Thyroid Hormones

The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine , also known as tetraiodothyronine or T4, and triiodothyronine , also known as T3. These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria resulting in increased ATP production. In the nucleus, T3 i T4 activate genes involved in energy production and glucose oxidation. This results in increased rates of metabolism and body heat production, which is known as the hormone’s calorigenic effect.

T3 i T4 release from the thyroid gland is stimulated by thyroid-stimulating hormone (TSH) , which is produced by the anterior pituitary. TSH binding at the receptors of the follicle of the thyroid triggers the production of T3 i T4 from a glycoprotein called thyroglobulin . Thyroglobulin is present in the follicles of the thyroid, and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported into the thyroid follicle from the bloodstream. A peroxidase enzyme then attaches the iodine to the tyrosine amino acid found in thyroglobulin. T3 has three iodine ions attached, while T4 has four iodine ions attached. T3 i T4 are then released into the bloodstream, with T4 being released in much greater amounts than T3. As T3 is more active than T4 and is responsible for most of the effects of thyroid hormones, tissues of the body convert T4 to T3 by the removal of an iodine ion. Most of the released T3 i T4 becomes attached to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unattached hormone begin to decline. In this way, a week’s worth of reserve hormone is maintained in the blood. Increased T3 i T4 levels in the blood inhibit the release of TSH, which results in lower T3 i T4 release from the thyroid.

The follicular cells of the thyroid require iodides (anions of iodine) in order to synthesize T3 i T4. Iodides obtained from the diet are actively transported into follicle cells resulting in a concentration that is approximately 30 times higher than in blood. The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to synthesize T3 i T4 hormones. The thyroid gland enlarges in a condition called goiter , which is caused by overproduction of TSH without the formation of thyroid hormone. Thyroglobulin is contained in a fluid called colloid, and TSH stimulation results in higher levels of colloid accumulation in the thyroid. In the absence of iodine, this is not converted to thyroid hormone, and colloid begins to accumulate more and more in the thyroid gland, leading to goiter.

Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism , underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism , the overproduction of thyroid hormones, can lead to an increased metabolic rate and its effects: weight loss, excess heat production, sweating, and an increased heart rate. Graves’ disease is one example of a hyperthyroid condition.

Hormonal Control of Blood Calcium Levels

Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result.

Blood calcium levels are regulated by parathyroid hormone (PTH) , which is produced by the parathyroid glands, as illustrated in Figure 37.12. PTH is released in response to low blood Ca 2+ levels. PTH increases Ca 2+ levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca 2+ from bone into the blood. PTH also inhibits osteoblasts, reducing Ca 2+ deposition in bone. In the intestines, PTH increases dietary Ca 2+ absorption, and in the kidneys, PTH stimulates reabsorption of the CA 2+ . While PTH acts directly on the kidneys to increase Ca 2+ reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.

Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).

The hormone calcitonin , which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.

Hormonal Regulation of Growth

Hormonska regulacija potrebna je za rast i replikaciju većine stanica u tijelu. Growth hormone (GH) , produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Hormon rasta ima izravne i neizravne mehanizme djelovanja. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. To rezultira prelaskom većine tkiva s korištenja glukoze kao izvora energije na korištenje masnih kiselina. This process is called a glucose-sparing effect . In another direct mechanism, GH stimulates glycogen breakdown in the liver the glycogen is then released into the blood as glucose. Razina glukoze u krvi raste jer većina tkiva koristi masne kiseline umjesto glukoze za svoje energetske potrebe. Povećanje razine glukoze u krvi posredovano GH naziva se dijabetogenim učinkom jer je slično visokim razinama glukoze u krvi koje se viđaju kod dijabetes melitusa.

The indirect mechanism of GH action is mediated by insulin-like growth factors (IGFs) or somatomedins, which are a family of growth-promoting proteins produced by the liver, which stimulates tissue growth. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in Figure 37.13. This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by growth hormone-inhibiting hormone (GHIH) , also called somatostatin.

A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in pituitary dwarfism , in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to gigantism in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to acromegaly , a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.

Hormonal Regulation of Stress

When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the “fight-or-flight” response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing up.

Evolucijska veza

Fight-or-Flight Response

Interactions of the endocrine hormones have evolved to ensure the body’s internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger.

However, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system’s high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water. The mechanisms to maintain homeostasis that are described here are those observed in the human body. However, the fight-or-flight response exists in some form in all vertebrates.

The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH) , which is produced by the anterior pituitary.

Short-term Stress Response

When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. How do these hormones provide a burst of energy? Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.

Watch this Discovery Channel animation describing the flight-or-flight response.

Long-term Stress Response

Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids . Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism. There are two main corticosteroids: glucocorticoids such as cortisol , and mineralocorticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoids primarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects.

Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.

Hypersecretion of glucocorticoids can cause a condition known as Cushing’s disease , characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison’s disease , which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.