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Titolo:
Acetylcholine release from cat carotid bodies
Autore:
Fitzgerald, RS; Shirahata, M; Wang, HY;
Indirizzi:
Johns Hopkins Med Inst, Dept Environm Hlth Sci, Div Physiol, Baltimore, MD21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 iol, Baltimore, MD21205 USA Johns Hopkins Med Inst, Dept Physiol, Baltimore, MD 21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 ol, Baltimore, MD 21205 USA Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 ed, Baltimore, MD 21205 USA Johns Hopkins Med Inst, Dept Anesthesiol Crit Care Med, Baltimore, MD 21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 ed, Baltimore, MD 21205 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 841, anno: 1999,
pagine: 53 - 61
SICI:
0006-8993(19990911)841:1-2<53:ARFCCB>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
BODY CHEMORECEPTORS; MUSCARINIC RECEPTORS; SUBSTANCE-P; HYPOXIA; DOPAMINE; RESPONSES; RABBIT; EXCITATION; LOCALIZATION; HYPERCAPNIA;
Keywords:
acetylcholine; carotid body; cholinergic receptor; cholinergic stimulation; hypoxia; HPLC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Fitzgerald, RS Johns Hopkins Univ, SHPU, EHS, 615 N Wolfe St, Baltimore, MD 21205 USA Johns Hopkins Univ 615 N Wolfe St Baltimore MD USA 21205 SA
Citazione:
R.S. Fitzgerald et al., "Acetylcholine release from cat carotid bodies", BRAIN RES, 841(1-2), 1999, pp. 53-61

Abstract

Hypoxia, hypercapnia and acidosis stimulate the carotid body (CB) sending increased neural activity via a branch of the glossopharyngeal nerve to nucleus tractus solitarius; this precipitates an impressive array of cardiopulmonary, endocrine and renal reflex responses. However, the cellular mechanisms by which these stimuli generate the increased CB neural output are onlypoorly understood. Central to the understanding of these mechanisms is thedetermination of which agents are released within the CB in response to hypoxia, and serve as the stimulating transmitter(s) for chemosensory nerve endings. Acetylcholine (ACh) has been proposed as such an agent from the outset, but this proposal has been, and remains, controversial. The present study tests two hypotheses: (1) The CB releases ACh under normoxic/normocapnic conditions; and (2) The amount released increases during hypoxia and other conditions known to increase neural output from the CB, These hypotheses were tested in 12 experiments in which both CBs were removed from the anesthetized cat and incubated at 37 degrees C in a physiological salt solution while the solution was bubbled with four different concentrations of oxygenand carbon dioxide. The incubation medium was exchanged at 10 min intervals for 30 min (three periods of incubation). The medium was analyzed with high performance liquid chromatography-electrochemical detection for ACh content. Normoxic/normocapnic conditions (21% O-2/6% CO2) produced a total of 0.639 +/- 0.106 pmol/150 mu l (mean +/- S.E.M.; n = 12). All stimulating conditions produced larger total outputs: 4% O-2/2% CO2 produced 1.773 +/- 0.46 pmol/150 mu l; 0% O-2/5% CO2, 0.868 +/- 0.13 pmol/150 mu l; 4% O-2/10% CO2, 1.077 +/- 0.21 pmol/150 mu l. These three amounts were significantly greater than the normoxic/normocapnic condition, but indistinguishable among themselves. Further, the amount of ACh released did not diminish over the 30min of stimulation. These data support the concept that during hypoxia AChfunctions as a stimulating transmitter in the CB, and are consistent with the earlier reports of cholinergic enzymes and receptors found in the CB. (C) 1999 Published by Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 10:26:30