Pathogenetic and therapeutic relevance of cardiovascular pressor reactivity to norepinephrine in human hypertension.

Abstract

In normotensive humans with a positive family history of essential hypertension, blood pressure (BP) is often dysregulated. Body sodium, blood volume, plasma angiotensin II (AngII), epinephrine and norepinephrine (NE), their responses to changes in sodium intake or posture, as well as baroreflex function, beta-receptor-mediated cardiac responsiveness, and the responsiveness of BP to AngII appear to be largely unaltered. However, the responsiveness of BP to NE is commonly exaggerated. An increase in potassium intake may improve the NE hyperreactivity and concomitantly lower BP within the "normotensive" range. Therefore, a selective vascular NE hyperreactivity relative to existing sympathetic activity seems to be a common familial abnormality predisposing for the development of essential hypertension. In borderline or established essential hypertension, an inappropriate vascular reactivity relative to sympathetic activity probably complements other mechanisms contributing to the maintenance of hypertension. Various antihypertensive treatments may lower BP at least in part by improving cardiovascular NE (hyper)reactivity without provoking an equivalent rise in sympathetic activity. These include dietary potassium supplementation, thiazide-type agents, indapamide, calcium channel blockers, postsynaptic alpha 1-blockers, and AngII converting enzyme inhibitors.