Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects - Role of endothelium-derived nitric oxide

Background-Several nonpharmacological interventions, including exercise, ar e recommended in primary prevention of hypertension and other cardiovascula r diseases in which the pathogenetic role of endothelial dysfunction has be en suggested. We studied the effects of long-term aerobic exercise on endot helial function in patients with essential hypertension. Methods and Results-The forearm blood flow was measured by strain-gauge ple thysmography. The responses of forearm vasculature to acetylcholine were sm aller in the hypertensive patients than in the normotensive subjects. There was no significant difference in forearm vascular responses to isosorbide dinitrate in the normotensive and hypertensive subjects. We evaluated the e ffects of physical exercise for 12 weeks on forearm hemodynamics in untreat ed patients with mild essential hypertension who were divided randomly into an exercise group (n=10) and a control group (n=7). After 12 weeks, the fo rearm blood flow response to acetylcholine increased-significantly, from 25 .8+/-9.8 to 32.3+/-11.2 mL.min(-1). 100 mL tissue(-1) (P<0.05), in the exer cise group but not in the control group. The increase in the forearm blood flow after isosorbide dinitrate was similar before and after 12 weeks of fo llow-up in both groups. The infusion of N-G-monomethyl-L-arginine abolished the exercise-induced enhancement of forearm vasorelaxation evoked by acety lcholine in the exercising group. In normotensive subjects also, long-term aerobic exercise augmented acetylcholine-stimulated nitric oxide release. Conclusions-These findings suggest that long-term physical exercise improve s endothelium-dependent vasorelaxation through an increase in the release o f nitric oxide in normotensive as well as hypertensive subjects.