Lahiri, S; Buerk, DG; Osanai, S; Mokashi, A; Chugh, DK

Journal of the Autonomic Nervous System [J. AUTON. NERV. SYST.], vol. 66, no. 1-2, pp. 1-6, Sep 1997

This study was done using high P sub(CO) (> 500 Torr at P sub(O2) of 120 Torr) in the carotid body perfusate in vitro, and recording simultaneously the activity of the whole carotid sinus nerve (CSN) and VO sub(2) of the carotid body. In the cascade of excitation of CSN by high P sub(CO) in the dark, Ca super(2+) effects occur at the level of neurosecretion after the level of oxygen consumption, according to the following scheme: CO-hypoxia arrow right VO sub(2) decrease arrow right K super(+) conductance decrease arrow right cell depolarization arrow right cytosolic Ca super(2+) rise arrow right neurosecretion arrow right neural discharge. Thus, a part of the hypothesis was that [Ca super(2+)] decrease, being a downstream event, may not affect VO sub(2) of the carotid body. Also, to determine to what extent the intracellular calcium stores contribute to cystolic [Ca super(2+)] and chemosensory discharge with high P sub(CO), we tested the effect of interruption of perfusate flow with medium nominally free of [Ca super(2+)] on CSN excitation and VO sub(2) of the carotid body with and without high P sub(CO). High P sub(CO) in the dark decreased carotid body VO sub(2), independent of [Ca super(2+)] sub(o). CSN excitation was always enhanced by high P sub(CO), and its sensitivity to perfusate flow interruption. Also, nominally Ca super(2+)-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 Ca super(2+) is released from intracellular stores, because CO has no other way to excite the chemoreceptors than by acting on the intracellular stores.