gms | German Medical Science

Impaired endothelium dependent NO mediated vasodilation is a cardinal feature of essential hypertension and may precede the increase in blood pressure. We sought to determine whether transport of the NO precursor L-arginine is related to decreased endothelial function and to the development of essential hypertension.

Using a complementary approach we assessed L-arginine uptake in the forearm during a steady-state intra-arterial infusion of [3H] L-arginine and in peripheral blood mononuclear cells isolated from hypertensive subjects (EH; n=8) and two groups of healthy volunteers with (PFH; n=10) and without (NFH; n=10) a family history of hypertension. Forearm blood flow response to acetylcholine and sodium-nitroprusside was measured by plethysmography both before and after supplemental intraarterial infusion of L-arginine (10mmol/min)..

In vivo and in vitro L-arginine transport was substantially reduced in EH and PFH compared to NFH (p<0.01 for both). Forearm blood flow response to acetylcholine was reduced in EH and PFH compared to NFH (mean ± SEM: 10.6 ± 0.75 vs 10.3 ± 1.32 vs 15.6 ± 1.06 ml/min/100ml, respectively; p<0.05). The response to sodium-nitroprusside was similar in all groups. L-arginine supplementation improved the response to acetylcholine only in subjects with EH and PFH (p<0.05, for both).

For the first time we demonstrate that similar to their hypertensive counterparts, normotensive individuals at high risk for the development of hypertension are characterized by impaired L-arginine transport and endothelial function. Reduced L-arginine transport may represent the link between a defective L-arginine-nitric oxide pathway and the onset of essential hypertension.