THAPSIGARGIN ENHANCES CAROTID-BODY CHEMOSENSORY DISCHARGE IN RESPONSETO HYPOXIA IN ZERO [CA2- EVIDENCE FOR INTRACELLULAR CA2+ RELEASE(](E))

To test the hypothesis that Ca2+ is released from intracellular store in the carotid body glomus cells during hypoxia, we stimultaneously me asured chemosensory discharge and tissue PO2 of perfused-superfused ca t carotid body before and during flow interruption in the presence and absence of extracellular [Ca2+] with and without thapsigargin (1-10 m u M). Ca2+-free solution increased the latency of sensory response, an d decreased the rate of rise and peak activity but thapsigargin signif icantly influenced these responses, without affecting oxygen consumpti on. Since thapsigargin depletes the intracellular Ca2+ store, and sinc e Ca2+ is needed for the sensory discharge, these results suggest that intracellular release and influx of Ca2+ occur during hypoxia.