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- W4246247907 abstract "This study was done using high PCO (>500 Torr at PO2 of 120 Torr) in the carotid body perfusate in vitro, and recording simultaneously the activity of the whole carotid sinus nerve (CSN) and V̇O2 of the carotid body. In the cascade of excitation of CSN by high PCO in the dark [light eliminated the excitation; S. Lahiri, News Physiol. Sci. 9 (1992) 161–165], Ca2+ effects occur at the level of neurosecretion after the level of oxygen consumption, according to the following scheme: CO-hypoxia→V̇O2 decrease→K+ conductance decrease→cell depolarization→cytosolic Ca2+ rise→neurosecretion→neural discharge. Thus, a part of the hypothesis was that [Ca2+] decrease, being a downstream event, may not affect V̇O2 of the carotid body. Also, to determine to what extent the intracellular calcium stores contribute to cystolic [Ca2+] and chemosensory discharge with high PCO, we tested the effect of interruption of perfusate flow with medium nominally free of [Ca2+] on CSN excitation and V̇O2 of the carotid body with and without high PCO. High PCO in the dark decreased carotid body V̇O2, independent of [Ca2+]o. CSN excitation was always enhanced by high PCO, and its sensitivity to perfusate flow interruption. Also, nominally Ca2+-free solution increased the latency and decreased the rate of rise and peak activity of CSN during interruption of perfusate flow, but CO augmented the responses. This reversal effect by CO suggests that Ca2+ is released from intracellular stores, because CO has no other way to excite the chemoreceptors than by acting on the intracellular stores." @default.
- W4246247907 created "2022-05-12" @default.
- W4246247907 date "2006-12-01" @default.
- W4246247907 modified "2023-10-14" @default.
- W4246247907 title "Sponsors" @default.
- W4246247907 doi "https://doi.org/10.1016/s0161-813x(06)00268-3" @default.
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