Abstract
The role of calcium in angiotensin II (Ang II)-induced vasoconstriction was investigated, using two models, the pithed rat and rat isolated aortic strips. In the pithed rat the increase in diastolic blood pressure elicited by Ang II consisted of an interaction with the sympathetic nervous system involving presynaptically released noradrenaline and of a direct stimulation of postsynaptic Ang II-receptors on vascular smooth muscle. This latter effect proved to be only partially dependent upon the influx of extracellular calcium ions. In rat isolated aortic strips Ang II-induced contractions did not contain an adrenergic component, and almost complete suppression of the response to Ang II could be observed after calcium entry blockade and also in a calcium-'free' medium. The difference in sensitivity to calcium antagonists in vivo and in vitro may be explained by the type of blood vessels involved.
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