Stimulation of vascular postsynaptic alpha 1-adrenoceptors by noradrenaline, released by angiotensin II in pithed rat preparations.

The influence of the sympathetic nervous system and of its adjacent adrenoceptors in the vasoconstriction induced by angiotensin II was studied in pithed rat preparations. The vasoconstriction induced by angiotensin II in high doses was impaired by reserpine pretreatment but not by bilateral adrenalectomy. These findings suggest that part of the pressor response of high doses of angiotensin II is caused by the liberation of endogenous noradrenaline from the sympathetic nerve endings, but not by that of adrenaline from the adrenal medulla. The vasoconstrictor effect of high doses of angiotensin II was depressed by the alpha 1-adrenoceptor antagonist prazosin, but not by the alpha 2-adrenoceptor antagonist yohimbine. A possible role of the sympathetic ganglia in the pressor activity of angiotensin could be ruled out by appropriate blockade of cholinergic transmission. In higher doses, angiotensin II causes vasoconstriction which is mediated partly by the release of noradrenaline from sympathetic nerve endings, leading to activation of predominantly postsynaptic alpha 1-adrenoceptors.