Angiotensin II-induced increase in slowly exchanging 45Ca2+ in relation to contractile responses of rat and guinea-pig aorta
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To gain more information about sources of activator Ca2+ involved in the contraction of rat and guinea-pig aorta evoked by angiotensin II and their sensitivity to Ca 2+ entry blockers, measurement of slowly exchanging 45Ca2+ was established. A more physiological procedure was used, replacing La3+- and EGTA- containing solutions by a normal Ca2+-containing buffer. It was demonstrated that the angiotensin 11-induced increase in slowly exchanging 45Ca2+ in rat aorta was incompletely (by approximately 60%–70%) inhibited by the organic Ca2+ entry blockers nifedipine, verapamil and diltiazem and by other Ca+ entry blocking compounds like CoCl2 and chlorpromazine. 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8) was able to inhibit the angiotensin II-induced increase in 45Ca2+ content completely, but this may be an intracellular storage effects. By contrast, the organic Ca2+ entry blockers completely inhibited that part of the angiotensin II-induced contraction of rat aorta which was dependent upon extracellular Ca2+.
In guinea-pig aorta, the increase in 45Ca2+ content elicited by angiotensin 11 could be completely suppressed by all compounds under study. The results of these experiments correlated well with data from the functional experiments in guinea-pig aorta. In both preparations the release of Ca 2+ from a rapidly as well as a slowly exchanging intracellular pool appears to contribute to the contractile response elicited by angiotensin 11.
Key words45Ca2+ Angiotensin II Calcium entry blockers Rat aorta Guinea-pig aorta
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