Altered vasodilator and endothelium‐dependent responses in hypertension

Abstract

AbstractA compromised ability to relax has been described as a characteristic of vascular smooth muscle from animal models of hypertension. Since the discovery that many vasodilators act via the release of an endothelium‐derived relaxant factor (EDRF), studies have been designed to assess whether endothelium‐dependent vs. ‐independent relaxations are impaired in the hypertensive state. A decreased maximal relaxation for such endothelium‐dependent vasodilators as acetylcholine, A23187, and histamine exists in both large conduit and resistance vessels from hypertensive animals compared to their normotensive counterparts. Endothelium‐independent vasodilators (i.e., sodium nitroprusside) typically achieve similar maximal percent relaxations in hypertensive vs. normotensive vascular preparations. This defect for endothelium‐dependent vasodilators has been described in vessels from genetic, renal, mineralocorticoid, and coarctation models of hypertension. An altered endothelium‐dependent relaxation could be a corollary of the documented structural changes which occur in hypertension although it remains to be determined if there exists an abnormal coupling between EDRF and its putative receptor in vascular smooth muscle. Several complexities hamper interpretation of altered endothelium‐dependent responses in hypertersion such as regional vascular differences, suitability of reference endothelium‐independent vasodilators, and endothelium‐dependent contractile responses elicited by acetylcholine.