ROLE OF SHEAR-STRESS AND ENDOTHELIAL PROSTAGLANDINS IN FLOW-INDUCED AND VISCOSITY-INDUCED DILATION OF ARTERIOLES INVITRO

We have studied the effect of changes in shear stress on diameter of isolated arterioles of rat cremaster muscle. The steady-state active diameter of arterioles at a constant perfusion pressure (60 mm Hg) was 80+/-1.2 mum. The vessels' passive diameter (Ca2+-free solution) was 156+/-1.8 mum. Changes in shear stress were induced either by an increase in flow (velocity) or by an increase in viscosity of the perfusion solution. At a constant perfusion pressure, the stepwise increase in perfusion flow (0-80 mul/min in 10-mul/min steps) elicited, with a delay of almost-equal-to 20 seconds, a gradual increase in diameter up to 46%. At a constant 20-mul/min flow rate, increases in viscosity of the perfusate (2%, 4%, and 6% dextran [molecular weight, 77,800]) caused a gradual vasodilation up to 22%. Varying flow and viscosity of the perfusate simultaneously resulted in an upward shift of the flow-diameter curve. Both flow- and viscosity-induced dilations were eliminated by the removal of the endothelium of arterioles (by air) or were inhibited by indomethacin (10(-5) M). The efficacy and specificity of these inhibitory treatments were assessed with vasoactive agents whose action, with regard to endothelial mediation, has been determined previously. The arteriolar dilation maintained calculated wall shear stress close to control values during increases in How and/or viscosity of the perfusate, but when the dilation was inhibited by removal of the endothelium or by indomethacin, wall shear stress increased significantly in a cumulative manner. We conclude that, in isolated arterioles of cremaster muscle, the dilation to increased How (velocity) or viscosity of the perfusate is the result of an increase in shear stress that elicits the release of vasodilator prostaglandins from the endothelium.