Transvascular albumin leakage and forearm vasodilatation to acetylcholine in essential hypertension.

The impact of hypertension on microvascular permeability and nitric oxide-mediated endothelial vasomotion in humans has been studied by measuring either the transcapillary albumin escape rate (TERalb, a measure of permeability through systemic capillary endothelium where most of the albumin permeation takes place) and forearm vasodilatation to locally infused acetylcholine (used as a probe for the nitric oxide-releasing potential of arteriolar endothelial cells). It is unknown, however, how the two parameters relate to each other in the same hypertensive subject. This piece of evidence may enhance our understanding about the relative effect of hypertension on two biological functions (ie, permeability and nitric oxide-mediated vasomotion), both dependent on vascular endothelium, and also may allow to appreciate in greater detail the profile of parameters frequently used as markers of microvascular dysfunction in human hypertension. For these reasons, TERa1b (the 1-h decline rate of intravenous 125I-albumin) and forearm vasodilatation (strain gauge venous plethysmography) to graded intraarterial acetylcholine infusion were measured in 44 never-treated men with uncomplicated essential hypertension, and 15 male normotensive controls with comparable age, lipids, and proportion of current smokers. TERalb was increased in patients, whereas acetylcholine-mediated vasodilatation did not differ significantly between the two groups, indicating a heterogeneous impact of elevated blood pressure on capillary permeability and endothelial vasomotion in still uncomplicated mild to moderate essential hypertensive patients. The dissociation between TERalb and forearm responsiveness to acetylcholine also demonstrates that different endothelial-dependent biologic parameters do not behave uniformly in human hypertension.