EFFECTS OF CAPTOPRIL AND ENALAPRIL ON INTRACELLULAR CA2-MUSCLE CELL( IN VASCULAR SMOOTH)

AIM: To determine whether angiotensin-converting enzyme inhibitors can affect Ca2+ handling in cultured aortic smooth muscle cells (ASMC) di rectly. METHODS: Cultured ASMC derived from rat aorta were loaded with the intracellular Ca2+ ([Ca](2+)(i)) fluorescent indicator Furs 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-, norepinephri ne (NE)-, and angiotensin II (Ang)-induced [Ca2+](i) increases were en hanced 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). Capto pril (Cap) and enalapril (Ena) had no inhibitory effect on KCl-, NE-, and Ang-induced [Ca2+](i) increases in ASMC of WKY. Cap and Ena inhibi ted KCl-, NE-, and Ang-increased [Ca2+](i) in ASMC of SHR (210 +/- 7, 194 +/- 6, and 201 +/- 6 nmol . L(-1), respectively). Ena and nifedipi ne similarly decreased KCl-, NE-, and Ang-increased [Ca2+](i). CONCLUS ION: Cap blocked KCl-, NE-, and Ang-increased ([Ca2+](i)) via a voltag e-dependent Ca2+ channel of which function and specificity was altered in ASMC of SHR.