Charybdotoxin (ChTX), a venom protein, suppresses Ca2+-activated K+ (K
-Ca(+)) currents in the glomus cell of neonatal rat carotid body. If i
t works similarly for cat carotid body chemoreceptors, charybdotoxin i
s expected to stimulate the chemosensory discharge during normoxia, an
d particularly hypoxia and hypercapnia. We studied the effects of char
ybdotoxin (20-40 nM) in vitro (perfused/superfused) on the cat carotid
chemosensory discharge, and simultaneously tissue PO2 (PtiO(2)), as a
measure of positive control. ChTX (20 nM) only increased PtiO(2) and
decreased carotid chemosensory discharge during hypoxia, indicating va
sodilation. We conclude that K-Ca(+) channels do not appear to play a
significant role in chemotransduction in the cat carotid body.