EFFECT OF ANGIOTENSIN-II ON NORADRENALINE RELEASE IN THE HUMAN FOREARM

Objective: The aim was to test the hypothesis that in normal humans an giotensin II would stimulate local release of noradrenaline under basa l conditions or during a sympathetic stimulus provided by lower body n egative pressure (LBNP). Methods: Nine healthy volunteers received int ra-arterial infusions of angiotensin II, 5 ng.min(-1), into the non-do minant forearm. Forearm blood flow (strain gauge plethysmography) and regional noradrenaline spillover (using the tracer methodology of Esle r) were measured during angiotensin II alone, LBNP alone, and LBNP plu s angiotensin II. Results: Angiotensin II and LBNP decreased forearm b lood flow comparably: from 3.1(SD 1.5) to 2.4 (0.9) ml.100 g(-1).min(- 1) during angiotensin II, p<0.05; and from 3.3(1.5) to 2.5(1.0) ml.100 g(-1) min(-1) during LBNP, p<0.05 (p=NS, A-II v LBNP). Angiotensin II had no effect on forearm venous noradrenaline or regional noradrenali ne spillover. LBNP increased venous noradrenaline outflow from the for earm, from 1.6(0.40) to 2.1(0.6) nmol.min(-1) (p<0.05), while regional noradrenaline spillover tended to increase, rising from 1.5(0.8) to 2 .0(1.0) nmol.100 ml(-1) min(-1). Angiotensin II did not enhance forear m blood flow or noradrenaline responses to LBNP. Conclusions: In the h uman forearm, mildly vasoconstrictor infusions of angiotensin II do no t increase local release of noradrenaline, either alone or during mild LBNP. At least under these conditions, angiotensin II would not appea r to be a potent influence on local sympathetic activity.