ATRIAL-NATRIURETIC-FACTOR POTENTIATES THE HUMAN FOREARM VASOCONSTRICTOR RESPONSE TO SYMPATHETIC-STIMULATION

1. Atrial natriuretic factor has been suggested to affect human sympat hetic nervous system activity. The interaction between atrial natriure tic factor and the sympathetic nervous system has not been fully eluci dated yet, but may occur at different sites. We studied this modulator effect at the level of the forearm vascular bed: the forearm vasocons trictor response was examined after alpha-adrenergic sympathetic stimu lation in healthy subjects during the locoregional administration of a trial natriuretic factor, sodium nitroprusside and placebo. As a sympa thetic stimulation test, the technique of the lower body negative pres sure (-20 mmHg) was used. 2. Lower body negative pressure increased th e forearm vascular resistance by +37+/-8% during concomitant intra-art erial infusion of placebo (n = 10). During a predilator state achieved by infusion of atrial natriuretic factor (10 ng min(-1) 100 ml(-1) fo rearm volume) into the brachial artery, lower body negative pressure s ubsequently induced a forearm vasoconstrictor response of +153+/-22% ( P < 0.05 versus placebo), whereas this was +64+/-14% when predilatatio n was achieved by infusion of an equipotent vasodilator dose of sodium nitroprusside (P > 0.1 versus placebo; P < 0.05 versus atrial natriur etic factor). The potentiation of the forearm vasoconstrictor response to lower body negative pressure by atrial natriuretic factor only occ urred in the experimental and not in the contralateral arm. According to calculations on simultaneously sampled arterial and venous plasma c atecholamine concentrations, the augmented forearm vasoconstrictor res ponse seemed not to be caused by an increased release of noradrenaline . 3. In a second experiment (n = 10), we demonstrated that atrial natr iuretic factor did not alter the forearm vasoconstrictor response to t he intra-arterial administration of exogenous noradrenaline, thereby e xcluding a postsynaptic modulation by atrial natriuretic factor. In th e presence of atrial natriuretic factor, the subsequent infusion of tw o dosages of noradrenaline (0.1 and 1.0 ng min(-1) 100 ml(-1) forearm volume) increased the forearm vascular resistance by +118+/-29% and +3 87+/-79%, respectively, whereas these numbered +129+/-18% and +316+/-4 1% when atrial natriuretic factor was replaced by an equipotent dose o f sodium nitroprusside. 4. We conclude that atrial natriuretic factor potentiates the forearm vasoconstrictor response to alpha-adrenergic s ympathetic stimulation in man, and that this effect may be located at the level of the forearm vascular bed. This potentiation cannot be exp lained by an increased vascular alpha-adrenergic sensitivity. More det ailed studies are needed to analyse the effects of atrial natriuretic factor on local noradrenaline kinetics to elucidate influences on symp athetic neurotransmission.