Hatem S N, Sweeten T, Vetter V, Morad M
Department of Pharmacology, Georgetown University, Washington, DC 20007.
Am J Physiol. 1995 Mar;268(3 Pt 2):H1195-201. doi: 10.1152/ajpheart.1995.268.3.H1195.
The characteristics of Ca2+ signaling in fura 2-loaded whole cell-clamped myocytes obtained from samples of human atrial appendages of 3-day to 4-yr-old patients were examined. In isolated myocytes, activation of Ca2+ current (ICa) (2.47 +/- 0.23 pA/pF) at 0 mV elicited sizable intracellular Ca2+ (Cai) transients (240 +/- 45 nM), which were caused by the release of Ca2+ from intracellular stores as they were suppressed in the presence of ryanodine or caffeine. The voltage dependence of both Cai transients and ICa were similar and bell shaped. The rate of release of Ca2+, normalized for the maximal Ca2+ release, increased with age, indicating increased efficiency of Ca2+ signaling in more mature myocytes. The results suggest that ICa-gated release of Ca2+ from the sarcoplasmic reticulum is the primary mechanism regulating the signaling of contraction in early postnatal as well as older human atrial myocytes.
对从3日龄至4岁患者的人心房附件样本中获取的、用fura 2加载的全细胞钳制心肌细胞中的Ca2+信号特征进行了检测。在分离的心肌细胞中，0 mV时Ca2+电流（ICa）（2.47±0.23 pA/pF）的激活引发了相当大的细胞内Ca2+（Cai）瞬变（240±45 nM），这是由细胞内钙库释放Ca2+所致，因为在存在兰尼碱或咖啡因的情况下这种瞬变受到了抑制。Cai瞬变和ICa的电压依赖性相似，均呈钟形。以最大Ca2+释放量进行归一化的Ca2+释放速率随年龄增加而升高，表明在更成熟的心肌细胞中Ca2+信号传导效率提高。结果提示，ICa门控的肌浆网Ca2+释放是调节出生后早期以及年长人心房肌细胞收缩信号传导的主要机制。
