DECREASED VASCULAR RELAXATION IN HYPERTENSION

Abstract

Relaxation of spirally cut aortic strips was diminished in vessels from both spontaneously hypertensive rats and renal hypertensive rats. Aortic relaxation was decreased in response to the cyclic nucleotides and the .beta.-adrenergic stimulant, isoproterenol, in both models of hypertension. Defective aortic relaxation also occurred with 2 other vasodilators, nitroglycerin and adenosine. Further evidence for a reduced relaxant ability of blood vessels from hypertensive rats was obtained by measuring aortic relaxation after exposure and subsequent removal of vascular contractile agonists. The time for aortic preparations from spontaneously hypertensive rats to relax to base-line tension after maximum contraction with norepinephrine, serotonin and KCl was significantly prolonged compared to recovery time for vessels from Kyoto Wistar normotensive rats. Treatment of the spontaneously hypertensive rat with reserpine, but not hydralazine, resulted in an improved ability of aortic preparations to relax. Defects in vascular relaxation may contribute to hypertension, and some antihypertensive drugs may improve or facilitate vascular relaxation.