Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.
Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.
复制标题
乙酰胆碱增加成年猫动脉化学感受器细胞的细胞内钙。
DOI:
10.1152/jn.1997.78.5.2388
复制
发表时间:
1997
期刊:
影响因子:
--
通讯作者:
Sham,JS
中科院分区:
文献类型:
--
作者:
Shirahata,M;Fitzgerald,RS;Sham,JS
Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham.Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.J. Neurophysiol.78: 2388–2395, 1997. 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+]iwas measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]iin ∼70% of clusters, and the responses to 1–300 μM 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+]iwas 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 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]iin 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+]iof cultured carotid body cells by activating neuronal nicotinic ACh receptors, 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+]iin response to ACh. Muscarinic receptors appear to play only a small role, if any.
登录
查看更多内容
DOI:
--
发表时间:
1952
期刊:
Acta Physiologica Scandinavica
影响因子:
--
作者:
S. Landgren;G. Liljestrand;Y. Zotterman
通讯作者:
Y. Zotterman
影响因子:
2.9
作者:
A. Ishida;K. Shimazaki;T. Terashima;N. Kawai
通讯作者:
N. Kawai
影响因子:
2.9
作者:
B. Dinger;C. González;K. Yoshizaki;S. Fidone
通讯作者:
S. Fidone
DOI:
--
发表时间:
1985-03
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
G. Grynkiewicz;M. Poenie;Roger Y. TsienB
通讯作者:
G. Grynkiewicz;M. Poenie;Roger Y. TsienB
DOI:
--
发表时间:
1987
期刊:
影响因子:
--
作者:
A. Obeso;S. Fidone;Constancio González
通讯作者:
Constancio González