Effects of captopril and enalapril on intracellular Ca2+ in vascular smooth muscle cell
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...
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Published in | Zhōngguó yàolĭ xuébào Vol. 17; no. 2; pp. 142 - 145 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Beijing
Science Press
01.03.1996
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0253-9756 |