摘要
目的:检测ACE抑制剂对主动脉平滑肌细胞内Ca^(2+)的影响。方法:用荧光标计和图象处理技术。结果:SHR细胞内Ca^(2+)以及KCl,NE和Ang在SHR细胞引起的Ca^(2+)增加多于WKY细胞。Cap和Ena不影响KCl和Ang在WKY细胞的作用,但Cap,Ena和Nif抑制KCl,NE和Ang在SHR细胞的作用。结论:Cap和Ena阻断功能和特异性已改变的电压依赖性钙通道。
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]i2+ ) 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). KC1-, norepinephrine (NE)-, and angiotensin II (Ang)-induced [Ca 2+ ]; 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 , respectively). Captopril (Cap) and enalapril (Ena) had no inhibitory effect on KC1-, NE-, and Ang-induced [Ca 2+ ]; increases in ASMC of WKY. Cap and Ena inhibited KC1-, NE-, and Ang-increased [Ca2+ ]; in ASMC of SHR (210 ±7, 194 ±6, and 201 ±6 nmol·L-1, respectively). Ena and nifedipine similarly decreased KC1-, NE-, and Ang-increased [Ca2+]i. CONCLUSION: Cap blocked KC1-, NE-, and Ang-increased ([Ca2 + ];) via a voltage-dependent Ca2 + channel of which function and specificity was altered in ASMC of SHR.
出处
《中国药理学报》
CSCD
1996年第2期142-145,共4页
Acta Pharmacologica Sinica
基金
supported by the National Natural Science Foundation of China,№ 39270779.
关键词
胸主动脉
血管平滑肌
钙
卡托普利
依那普利
thoracic aorta
cultured cells
inbred WKY rats
inbred SHR rats
calcium
angiotensin II
captopril
enalapril
nifedipine
Fura-2
