Impaired nitric oxide-mediated flow-induced dilation in arterioles of spontaneously hypertensive rats

Abstract

We tested the hypothesis that impairment of flow-dependent dilator mechanisms of skeletal muscle arterioles is one of the underlying reasons for the increased peripheral resistance in hypertension. Isolated, cannulated arterioles (≃55 μm) of gracilis muscle of 12-week-old spontaneously hypertensive (SH) and normotensive Wistar (NW) rats were investigated. At a constant perfusion pressure (80 mm Hg), the active diameters of NW and SH arterioles were 57.7±1.9 and 51.5±3.2 μm, whereas their passive diameters (Ca2+-free solution) were 113.6±2.9 and 101.7±2.9 μm, respectively. Flow-induced dilation was elicited by increases in flow of the perfusion solution from 0 to 25 μL/min in 5-μL/min steps. This response was significantly less in arterioles of SH compared with NW rats. For example, at 25-μL/min flow, the diameter of arterioles of SH rats was ≃56% less (P