Qi J H, Zhang L, Wang J, Wei P J, Gu P K, Jin Z J, Huang M Z, Wang H Y
Department of Pharmacology, Shanghai Second Medical University, China.
Zhongguo Yao Li Xue Bao. 1996 Mar;17(2):142-5.
To determine whether angiotensin-converting enzyme inhibitors can affect Ca2+ handling in cultured aortic smooth muscle cells (ASMC) directly.
Cultured ASMC derived from rat aorta were loaded with the intracellular Ca2+ ([Ca]2+i) fluorescent indicator Fura 2-AM and digital image processing technique was used.
Resting [Ca2+]i was greater in ASMC from SHR vs WKY (P < 0.01). KCl-, norepinephrine (NE)-, and angiotensin II (Ang)-induced [Ca2+]i increases were enhanced in ASMC of SHR vs WKY (220 +/- 6, 212 +/- 8, and 215 +/- 14 vs 199 +/- 6, 202 +/- 7, and 195 +/- 7 nmol.L-1, respectively). Captopril (Cap) and enalapril (Ena) had no inhibitory effect on KCl-, NE-, and Ang-induced [Ca2+]i increases in ASMC of WKY. Cap and Ena inhibited KCl-, NE-, and Ang-increased [Ca2+]i in ASMC of SHR (210 +/- 7, 194 +/- 6, and 201 +/- 6 nmol.L-1, respectively). Ena and nifedipine similarly decreased KCl-, NE-, and Ang-increased [Ca2+]i.
Cap blocked KCl-, NE-, and Ang-increased ([Ca2+]i) via a voltage-dependent Ca2+ channel of which function and specificity was altered in ASMC of SHR.
直接确定血管紧张素转换酶抑制剂是否能影响培养的主动脉平滑肌细胞（ASMC）中的钙离子处理。
用细胞内钙离子（[Ca]2+i）荧光指示剂Fura 2-AM加载源自大鼠主动脉的培养ASMC，并使用数字图像处理技术。
与WKY相比，SHR的ASMC中静息[Ca2+]i更高（P<0.01）。与WKY相比，SHR的ASMC中氯化钾、去甲肾上腺素（NE）和血管紧张素II（Ang）诱导的[Ca2+]i增加增强（分别为220±6、212±8和215±14 vs 199±6、202±7和195±7 nmol·L-1）。卡托普利（Cap）和依那普利（Ena）对WKY的ASMC中氯化钾、NE和Ang诱导的[Ca2+]i增加无抑制作用。Cap和Ena抑制SHR的ASMC中氯化钾、NE和Ang增加的[Ca2+]i（分别为210±7、194±6和201±6 nmol·L-1）。Ena和硝苯地平同样降低了氯化钾、NE和Ang增加的[Ca2+]i。
Cap通过电压依赖性钙通道阻断氯化钾、NE和Ang增加的（[Ca2+]i），该通道的功能和特异性在SHR的ASMC中发生了改变。
