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Titolo:
ACETYLCHOLINE INCREASES INTRACELLULAR CALCIUM OF ARTERIAL CHEMORECEPTOR CELLS OF ADULT CATS
Autore:
SHIRAHATA M; FITZGERALD RS; SHAM JSK;
Indirizzi:
JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT ENVIRONM HLTH SCI,615 N WOLFE ST BALTIMORE MD 21205 JOHNS HOPKINS MED INST,DEPT ENVIRONM HLTH SCI BALTIMORE MD 21205 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED BALTIMORE MD 21205 JOHNS HOPKINS MED INST,DEPT PHYSIOL BALTIMORE MD 21205 JOHNS HOPKINS MED INST,DEPT MED BALTIMORE MD 21205
Titolo Testata:
Journal of neurophysiology
fascicolo: 5, volume: 78, anno: 1997,
pagine: 2388 - 2395
SICI:
0022-3077(1997)78:5<2388:AIICOA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT CAROTID-BODY; I CELLS; GLOMUS CELLS; RECEPTORS; DIVERSITY; CHANNELS; RABBIT; LOCALIZATION; DOPAMINE; HYPOXIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
M. Shirahata et al., "ACETYLCHOLINE INCREASES INTRACELLULAR CALCIUM OF ARTERIAL CHEMORECEPTOR CELLS OF ADULT CATS", Journal of neurophysiology, 78(5), 1997, pp. 2388-2395

Abstract

Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+](i)) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+](i) was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37 degrees C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O-2-79% N-2. ACh (100 mu M) caused a marked increase in [Ca2+](i) in similar to 70% of clusters, and the responses to 1-300 mu M of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+](i) was dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 mu M). The effect of mecamylamine (100 mu M) was inhibitory but small. Moreover, the increase in [Ca2+](i) in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+](i) of cultured carotid body cells by activating neuronal nicotinic AChreceptors, leading to Ca2+ influx via nicotinic channels. In addition, other pathways such as Ca2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+ release from intracellular stores may participate in increasing [Ca2+](i) in responseto ACh. Muscarinic receptors appear to play only a small role, if any.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 10:01:31