Osanai S, Buerk D G, Mokashi A, Chugh D K, Lahiri S
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6085, USA.
Brain Res. 1997 Feb 7;747(2):324-7. doi: 10.1016/s0006-8993(96)01313-3.
Charybdotoxin (ChTX), a venom protein, suppresses Ca2+-activated K+ (K+(Ca)) currents in the glomus cell of neonatal rat carotid body. If it works similarly for cat carotid body chemoreceptors, charybdotoxin is expected to stimulate the chemosensory discharge during normoxia, and particularly hypoxia and hypercapnia. We studied the effects of charybdotoxin (20-40 nM) in vitro (perfused/superfused) on the cat carotid chemosensory discharge, and simultaneously tissue PO2 (PtiO2), as a measure of positive control. ChTX (20 nM) only increased PtiO2 and decreased carotid chemosensory discharge during hypoxia, indicating vasodilation. We conclude that K+(Ca) channels do not appear to play a significant role in chemotransduction in the cat carotid body.
芋螺毒素(ChTX)是一种毒液蛋白,可抑制新生大鼠颈动脉体球细胞中钙激活钾通道(K+(Ca))的电流。如果它对猫颈动脉体化学感受器的作用类似,那么芋螺毒素有望在常氧状态下,尤其是在低氧和高碳酸血症期间刺激化学感受性放电。我们在体外(灌注/超灌注)研究了芋螺毒素(20 - 40 nM)对猫颈动脉化学感受性放电的影响,并同时测量了组织氧分压(PtiO2)作为阳性对照。ChTX(20 nM)仅在低氧期间增加了PtiO2并减少了颈动脉化学感受性放电,表明血管舒张。我们得出结论,K+(Ca)通道似乎在猫颈动脉体的化学转导中不发挥重要作用。