Skeletal muscle arteriolar constriction to ANG II: evaluation of a myogenic component.

Abstract

This study addressed the hypothesis that an increase in blood pressure contributes to the overall constrictive response of skeletal muscle arterioles to angiotensin II (ANG II). Diameters of second-order arterioles (2A) and third-order arterioles (3A) in the rat cremaster muscle were quantitated after intravenous administration of ANG II. Hindquarter blood pressure was either allowed to increase or was maintained at normal levels. Constriction of 3A to bolus injection of ANG II was the same whether hindquarter pressure increased or not. However, the total vascular constrictive response of the cremaster muscle (based on 2A blood flow) and of the entire hindquarter (based on iliac arterial blood flow) to bolus ANG II was greater when hindquarter pressure was held constant. During slow infusion of ANG II, 3A constriction was unaffected by an abrupt decrease or increase in hindquarter pressure. However, an abrupt reduction of hindquarter pressure caused a significant decline in hindquarter vascular resistance. Thus an increase in blood pressure, whether rapid or gradual, does not influence 3A constriction to ANG II. However, in the entire hindquarter, a rapid rise in blood pressure opposes constriction to ANG II, whereas a gradual pressure rise evokes a mechanism that enhances constrictive response to the peptide.