@article{APS6377,
author = {Jian-Hua Qi and Lu Zhang and Jun Wang and Pei-Jing Wei and Pei-Kun Gu and Zheng-Jun Jin and Ming-Zhi Huang and Hong-Yuan Wang},
title = {Effects of captopril and enalapril on intracellular Ca2+ in vascular smooth muscle cell},
journal = {Acta Pharmacologica Sinica},
volume = {17},
number = {2},
year = {2016},
keywords = {},
abstract = {AIM: To determine whether angiotensin-converting enzyme inhibitors can affect Ca2+ handling in cultured aortic smooth muscle cells (ASMC) directly.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/6377}
}