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Thapsigargin enhances carotid body chemosensory discharge in response to hypoxia in zero [Ca2+]e: evidence for intracellular Ca2+ release
Journal article   Peer reviewed

Thapsigargin enhances carotid body chemosensory discharge in response to hypoxia in zero [Ca2+]e: evidence for intracellular Ca2+ release

S Lahiri, S Osanai, D G Buerk, A Mokashi and D K Chugh
Brain research, v 709(1), pp 141-144
12 Feb 1996
PMID: 8869566
url
https://doi.org/10.1016/0006-8993(95)01342-3View
Published, Version of Record (VoR) Open

Abstract

Animals Calcium - metabolism Calcium-Transporting ATPases - antagonists & inhibitors Carotid Body - drug effects Carotid Body - physiopathology Cats Chemoreceptor Cells - drug effects Chemoreceptor Cells - physiopathology Extracellular Space - metabolism Hypoxia - physiopathology Intracellular Membranes - metabolism Oxygen Consumption - drug effects Thapsigargin - pharmacology
To test the hypothesis that Ca2+ is released from intracellular store in the carotid body glomus cells during hypoxia, we stimultaneously measured chemosensory discharge and tissue PO2 of perfused-superfused cat carotid body before and during flow interruption in the presence and absence of extracellular [Ca2+] with and without thapsigargin (1-10 microM). Ca(2+)-free solution increased the latency of sensory response, and decreased the rate of rise and peak activity but thapsigargin significantly influenced these responses, without affecting oxygen consumption. Since thapsigargin depletes the intracellular Ca2+ store, and since Ca2+ is needed for the sensory discharge, these results suggest that intracellular release and influx of Ca2+ occur during hypoxia.

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