Impaired l -Arginine Transport and Endothelial Function in Hypertensive and Genetically Predisposed Normotensive Subjects

Abstract

Background-Impaired endothelium-dependent NO-mediated vasodilation is a key feature of essential hypertension and may precede the increase in blood pressure. We investigated whether transport of the NO precursor L-arginine is related to decreased endothelial function. Methods and Results-Radiotracer kinetics ([3 H]L-arginine) were used to measure forearm and peripheral blood mononuclear cell arginine uptake in hypertensive subjects (nϭ12) and in 2 groups of healthy volunteers with (nϭ15) and without (nϭ15) a family history of hypertension. In conjunction, forearm blood flow responses to acetylcholine and sodium nitroprusside were measured before and after a supplemental intra-arterial infusion of L-arginine. In vivo and in vitro measures of L-arginine transport were substantially reduced in the essential hypertension and positive family history groups compared with the negative family history group; however, no difference was detected in peripheral blood mononuclear cell mRNA or protein expression levels for the cationic amino acid transporter CAT-1. Plasma concentrations of L-arginine and N G ,N GЈ -dimethylarginine (ADMA) did not differ between groups. L-Arginine supplementation improved the response to acetylcholine only in subjects with essential hypertension and positive family history. Conclusions-Similar

Role of the nitric oxide metabolic pathway and prostanoids in the pathogenesis of endothelial dysfunction and essential hypertension in young men

“…Contrary to other investigators, Schlaich et al 38 did not find significant differences in plasma levels of ADMA and L-arginine between healthy and hypertensive subjects. 39 In our current study, we did not observe HTN-dependent differences in concentrations of ADMA, L-arginine or the L-arginine/ADMA ratio.…”

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“…Cardiac muscle fibers and coronary vascular beds express the enzyme endothelial NOS (Balligand et al, 1995). Numerous studies have shown that hypertension is accompanied by reduced endothelial function, which can be rescued to varying degrees by l-arginine supplementation (Schlaich et al, 2004;Higashi et al, 1995;Quyyumi et al, 1997;Lerman et al, 1998;Lekakis et al, 2002). l-Arginine is conditionally essential amino acid in the human diet.…”

Say NO to Obesity-Related Hypertension

“…51 We have previously shown that l-arginine transport, assessed both in vivo and in vitro, is reduced not only in hypertensive subjects but also in those that are genetically predisposed to hypertension. 64 Although this study did not specifically address obesity-related hypertension, hypertensive subjects had a greater body mass index than their normotensive counterparts. 64 A series of important questions arise from these observations.…”

“…64 Although this study did not specifically address obesity-related hypertension, hypertensive subjects had a greater body mass index than their normotensive counterparts. 64 A series of important questions arise from these observations. For example, does obesity per se reduce l-arginine transport only in a subset of Reduced nitric oxide (NO) bioavailability in obesity can augment sympathetic outflow which in the kidney can activate renal renin-angiotensin system (RAS).…”