Sato M, Ikeda K, Yoshizaki K, Koyano H
Department of Physiology, Akita University School of Medicine, Japan.
Brain Res. 1991 Jun 14;551(1-2):327-30. doi: 10.1016/0006-8993(91)90951-q.
Microscopic fluorometry was used to examine the effects of anoxia and cyanide (CN-) on cytosolic calcium [Ca2+]i of cultured carotid body (CB) glomus cells from newborn rabbits. Applications of high K+ and veratridine (VRT), a sodium channel activator, induced rapid and marked increases in [Ca2+]i. These effects were inhibited by D600 a calcium channel blocker. [Ca2+]i changes induced by VRT were also blocked by tetrodotoxin (TTX). Glomus cells exhibited a slow increase in [Ca2+]i in response to anoxia and CN-, and a slight decrease during hyperoxia. The effects of anoxia and CN- were blocked by D600 but not by TTX. We conclude that these stimuli induce calcium entry into glomus cells via voltage-dependent Ca2+ channels. Voltage-dependent Na+ channels were not involved.
采用显微荧光测定法研究缺氧和氰化物（CN-）对新生兔培养的颈动脉体（CB）球细胞胞质钙[Ca2+]i的影响。应用高钾和藜芦碱（VRT，一种钠通道激活剂）可诱导[Ca2+]i迅速且显著升高。这些效应被钙通道阻滞剂D600抑制。VRT诱导的[Ca2+]i变化也被河豚毒素（TTX）阻断。球细胞对缺氧和CN-的反应表现为[Ca2+]i缓慢升高，而在高氧期间略有下降。缺氧和CN-的效应被D600阻断，但未被TTX阻断。我们得出结论，这些刺激通过电压依赖性Ca2+通道诱导钙进入球细胞。电压依赖性Na+通道未参与其中。
