Key result
L-arginine infusion acts as a potent renal vasodilator without affecting glomerular filtration rate, an effect that is markedly blunted in patients with essential hypertension.
L-arginine infusion reveals that nitric oxide mediates renal vasodilation in humans, a mechanism that is impaired in essential hypertension.
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Indicates impaired NO-mediated renal vasodilation in hypertension; leaves open whether targeting this pathway improves outcomes.
Animal experiments have shown extensively that the endothelial generation of nitric oxide participates in the regulation of renal haemodynamics and function, probably as a factor modulating the effects of endogenous vasoconstrictors. Although the endothelial function of the systemic vasculature is assessed through the vasodilatory effect of acetylcholine, only L-arginine infusion is available for studies of the influence of nitric oxide on the renal circulation in humans. In addition to peripheral vessels, L-arginine is a potent renal vasodilator, having no effect on the glomerular filtration rate; and the renal relaxation induced by L-arginine is markedly blunted in patients with essential hypertension. A few studies showing the renal vasoconstrictor effect of an inhibitor of nitric oxide synthesis have been reported.
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A Mimran (1998) conducted a review in Essential hypertension. L-arginine infusion was evaluated. L-arginine infusion acts as a potent renal vasodilator without affecting glomerular filtration rate, an effect that is markedly blunted in patients with essential hypertension.
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