Forearm vasoconstriction in response to noradrenaline and N-G-monomethyl-L-arginine in essential hypertension

A role for abnormal NO production in essential hypertension remains controv ersial. Blunted vasoconstriction of forearm resistance vasculature in respo nse to N-G-monomethyl-L-arginine (L-NMMA; an inhibitor of NO biosynthesis), relative to the response to noradrenaline, has been reported in hypertensi ve patients and interpreted as evidence of I educed basal NO biosynthesis. We sought to determine whether reduced sensitivity of forearm vasculature t o the vasoconstrictor action of L-NMMA relative to that of noradrenaline is a consistent finding in essential hypertension. We studied a group of pati ents (n = 32; blood pressure 176 +/- 4/102 +/- 2 mmHg; means +/- S.E.M.) an d a group of healthy normotensive controls (n = 32; blood pressure 130 +/- 2/75 +/- 1 mmHg). Noradrenaline (60-240 pmol.min(-1)) and L-NMMA (1-4 mu mo l.min(-1)) were infused into the brachial artery, and forearm blood flow wa s measured by venous occlusion plethysmography. The effects of each vasocon strictor were similar in hypertensive and control subjects. The highest dos e of L-NMMA reduced forearm blood flow by 0.75 +/- 0.12 ml.min(-1).dl(-1) i n the control group and by 0.89 +/- 0.10 ml.min(-1).dl(-1) in the hypertens ive group. The study had 90% power (with P = 0.05) to detect a 10% differen ce in forearm blood flow response between the hypertensive and control grou ps. We conclude that reduced sensitivity of forearm resistance vasculature to the vasoconstrictor action of L-NMMA is not a universal feature of essen tial hypertension. This argues against a primary role for reduced basal NO biosynthesis in skeletal muscle resistance vessels in the pathogenesis of e ssential hypertension.