Original Article

Effects of captopril and enalapril on intracellular Ca2+ in vascular smooth muscle cell

Jian-Hua Qi, Lu Zhang, Jun Wang, Pei-Jing Wei, Pei-Kun Gu, Zheng-Jun Jin, Ming-Zhi Huang, Hong-Yuan Wang


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.

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