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Does captopril reduce Ang II-induced Ca2+ influx and vasoconstriction in rat aortic smooth muscle cells?
Does captopril reduce Ang II-induced Ca2+ influx and vasoconstriction in rat aortic smooth muscle cells?
Captopril and enalaprilat directly inhibit Ca2+ influx and vasoconstriction in vascular smooth muscle cells, suggesting therapeutic relevance beyond ACE inhibition.
May attenuate Ang II vasoconstriction in vascular smooth muscle; hypothesis-generating for direct effects beyond ACE inhibition in humans.
The effects of captopril on the response of cytosolic free Ca2+ concentration in cultured vascular smooth muscle cells of aortas from Wistar-Kyoto and spontaneously hypertensive rats to angiotensin II (Ang II) and bradykinin were studied using fura 2. Incubation with captopril for longer than 10 minutes caused a decreased response of cytosolic free Ca2+ to Ang II and bradykinin. Maximal effects of captopril were observed after a 40-minute incubation. The inhibitory effect of captopril was abolished in Ca(2+)-free medium, suggesting that captopril acts by blocking Ca2+ influx. Similar effects were observed with enalaprilat. Isometric contraction of aortic strips induced by Ang II in normotensive rats was reduced from 6.5 +/- 2.5 to 1.8 +/- 0.6 mN by a 40-minute incubation with 1 mumol/L captopril (P = .016). Enalaprilat similarly decreased the Ang II-induced contraction. Besides the inhibition of the angiotensin converting enzyme, direct effects of Ang II converting enzyme inhibitors on vascular contraction and Ca2+ influx in vascular smooth muscle cells may be of therapeutic relevance.
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Zhu et al. (1993) studied this question.
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