Angiotensin II. Adrenergic sympathetic constrictor action in humans

Angiotensin II (Ang II) facilitates adrenergic neurotransmission in normotensive and hypertensive subjects, whereas angiotensin-converting enzyme inhibitors have been shown to depress circulating catecholamine concentrations in some studies. We investigated the effect of local intra-arterial infusion of Ang II into the brachial artery of healthy volunteers during blockade of postsynaptic alpha-receptors with phentolamine. The response was compared with that seen with Ang II infused during nitroprusside administration at a dose designed to give a dilator response similar to that with phentolamine.

Ang II (6.25, 25, and 100 pmol/min) was infused alone and then together with sodium nitroprusside (4 micrograms/min) and phentolamine (40 micrograms/min) in eight healthy volunteers. Forearm blood flow was measured by strain-gauge plethysmography. The percentage reduction in forearm blood flow produced by Ang II 100 pmol/min in the phentolamine-predilated vascular bed was significantly lower than that seen in the sodium nitroprusside-predilated forearm bed (28.1 +/- 2.9% versus 52.9 +/- 4.2%; P = .006). Comparison of the rate of change of blood flow in response to quadrupling doses of Ang II during blockade of alpha-receptors with phentolamine and during nitroprusside administration was calculated from the mean slope of the regression line of log-transformed blood flow versus dose of Ang II. The mean slope during nitroprusside administration (-0.16 +/- 0.025) was significantly greater than that during blockade with phentolamine (-0.098 +/- 0.020) (P = .046).

We conclude that a significant part of the vasoconstrictive action of exogenous Ang II on forearm resistance vessels in humans is sympathetically mediated.