Role of the endothelium on the facilitatory effects of angiotensin I and angiotensin II on noradrenergic transmission in the caudal artery of the rat.

Perfusion of carbogen gas through the lumen of the rat caudal artery abolished the dilator response to acetylcholine (1 mumol 1(-1) in artery segments which had been precontracted with noradrenaline (50 nmol 1(-1]. Hence, it was assumed that gas perfusion was effective in removing the vascular endothelium. Angiotensin I (30 nmol 1(-1] and angiotensin II (10 nmol 1(-1] enhanced the responses of artery segments to field stimulation of their sympathetic nerves (0.5 Hz, 10 s). In arteries with an intact endothelium the ability of each peptide to enhance responses to stimulation was the same whether applied through the lumen or to the adventitial surface. Removal of the endothelium, by gas perfusion, did not significantly alter the facilitatory effects of extraluminally or intraluminally applied angiotensin I or angiotensin II. The converting enzyme inhibitor enalaprilat was equally effective in inhibiting the facilitatory effect of angiotensin I in the presence and absence of an intact endothelium. It is concluded that in the rat caudal artery, conversion of angiotensin I to angiotensin II does not depend on an intact endothelium and that the facilitatory effect of angiotensin II on noradrenergic neuroeffector transmission is not modified by, or dependent on, an intact endothelium.