Daily Aerobic Exercise Improves Reactive Hyperemia in Patients With Essential Hypertension

Abstract

The effects of long-term aerobic exercise on endothelial function in patients with essential hypertension remain unclear. To determine whether endothelial function relating to forearm hemodynamics in these patients differs from normotensive subjects and whether endothelial function can be modified by continued physical exercise, we randomized patients with essential hypertension into a group that engaged in 30 minutes of brisk walking 5 to 7 times weekly for 12 weeks (n20) or a group that underwent no activity modifications (control group, n7). Forearm blood flow was measured using strain-gauge plethysmography during reactive hyperemia to test for endothelium-dependent vasodilation and after sublingual nitroglycerin administration to test endothelium-independent vasodilation. Forearm blood flow in hypertensive patients during reactive hyperemia was significantly less than that in normotensive subjects (n17). Increases in forearm blood flow after nitroglycerin were similar between hypertensive and normotensive subjects. Exercise lowered mean blood pressure from 115.75.3 to 110.25.1 mm Hg (P0.01) and forearm vascular resistance from 25.63.2 to 23.22.8 mm Hg/mL per minute per 100 mL tissue (P0.01); no change occurred in controls. Basal forearm blood flow, body weight, and heart rate did not differ with exercise. After 12 weeks of exercise, maximal forearm blood flow response during reactive hyperemia increased significantly, from 38.44.6 to 47.14.9 mL/min per 100 mL tissue (P0.05); this increase was not seen in controls. Changes in forearm blood flow after sublingual nitroglycerin administration were similar before and after 12 weeks of exercise. Intra-arterial infusion of the nitric oxide synthase inhibitor N G-monomethyl-L-arginine abolished the enhancement of reactive hyperemia induced by 12 weeks of exercise. These findings suggest that through increased release of nitric oxide, continued physical exercise alleviates impairment of reactive hyperemia in patients with essential hypertension. (Hypertension. 1999;33[part II]:591-597.) Key Words: exercise, aerobic hyperemia, reactive nitroglycerin nitric oxide N G-monomethyl-L-arginine endothelium hypertension, essential R egular aerobic exercise by patients with essential hyper-tension is associated with beneficial changes in blood pressure, lipoprotein profile, glucose metabolism, and neuro-hormonal release. Recent epidemiological studies have shown that physical exercise reduces cardiovascular morbidity and mortality in the general population, including individuals with hypertension. 1,2 However, the mechanism underlying antihypertensive and antiatherogenic effects of exercise remains unclear. Several lines of evidence indicate impairment of endothe-lium-dependent vasorelaxation in the vessels of the forearm 3,4 and in the coronary 5 and renal 6,7 circulation of patients with essential hypertension. Recent experiments have demonstrated that continued exercise augmented vasodilation evoked by the endothelium-dependent vasodilator acetylcho-line in dogs 8 and rats,...

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

“…For example, Hagberg et al 32 found that regular exercise has the ability to reduce BP in approximately 75.0% of hypertensive patients and that training with moderate intensity seems to generate greater benefits than with high intensity, for such reductions. Higashi et al 4 observed a beneficial effect of regular aerobic exercise on blood pressure values for hypertensive patients.…”

“…The release of NO has been considered as a strong mediator for reactive hyperemia in peripheral arteries 4 . Thus, low levels of NOx observed in the TC + CC group, associated with the responses of BF among groups in the pre-training evaluation, are in agreement with other studies that have shown similar results 24 .…”

“…When eNOS is activated, the metabolism of L-arginine is increased generating the formation of L-citrulline and NO by endothelial cells [3][4][5] . Once produced, NO migrates to the vascular smooth muscle cell generating increased activity of guanylate cyclase, resulting in decreased calcium and vascular smooth muscle relaxation 5,6 .…”

Effects of exercise, diet and their combination on blood pressure

“…10 More recently, it has been suggested that improvement of endothelial function contributes to the reduction of blood pressure after training. [12][13][14] It is likely that the lowering of blood pressure by training is multifactorial and further studies are needed to elucidate the mechanisms. 9 Physical training, diet and blood pressure control…”

Non-pharmacological management of hypertension

“…Reduction of insulin resistance and improvement in endothelial function may also contribute. [19,20] Importantly, this reduction appeared to be independent of the intensity, frequency and type of exercise program. BP reduction was seen in normotensives also and was not inß uenced by initial weight.…”