EFFECT OF CO ON V-O2 OF CAROTID-BODY AND CHEMORECEPTION WITH AND WITHOUT CA2+

This study was done using high P-CO (> 500 Torr at P-O2 of 120 Torr) i n the carotid body perfusate in vitro, and recording simultaneously th e activity of the whole carotid sinus nerve (CSN) and (V) over dot (O2 ) of the carotid body. In the cascade of excitation of CSN by high P-C O in the dark [light eliminated the excitation; S. Lahiri, News Physio l. Sci. 9 (1992) 161-165], Ca2+ effects occur at the level of neurosec retion after the level of oxygen consumption, according to the followi ng scheme: CO-hypoxia --> (V) over dot decrease --> K+ conductance dec rease --> cell depolarization --> cytosolic Ca2+ rise --> neurosecreti on --> neural discharge. Thus, a part of the hypothesis was that [Ca2] decrease, being a downstream event, may not affect (V) over dot (O2) Of the carotid body. Also, to determine to what extent the intracellu lar calcium stores contribute to cystolic [Ca2+] and chemosensory disc harge with high P-CO, we tested the effect of interruption of perfusat e flow with medium nominally free of [Ca2+] on CSN excitation and (V) over dot (O2) of the carotid body with and without high P-CO. High P-C O in the dark decreased carotid body (V) over dot (O2), independent of [Ca2+](o). CSN excitation was always enhanced by high P-CO, and its s ensitivity to perfusate flow interruption. Also; nominally Ca2+-free s olution increased the latency and decreased the rate of rise and peak activity of CSN during interruption of perfusate flow, but CO augmente d the responses. This reversal effect by CO suggests that Ca2+ is rele ased from intracellular stores, because CO has no other way to excite the chemoreceptors than by acting on the intracellular stores. (C) Els evier Science B.V.