PRESERVATION OF VENULAR BUT NOT ARTERIOLAR SMOOTH-MUSCLE ALPHA-ADRENOCEPTOR SENSITIVITY DURING REDUCED BLOOD-FLOW

To compare arteriolar versus venular smooth muscle sensitivity to myogenic and metabolic inhibition during reduced blood pressure and flow, we measured the diameter of first-order venules (diameter, 230-mu-m) and arterioles (diameter, 156-mu-m) of the denervated, blood-perfused rat cremaster skeletal muscle that was suspended in a tissue bath. Sensitivity was determined for bath-added norepinephrine in the presence of yohimbine or prazosin to produce alpha-1- and alpha-2-adrenoceptor constriction, respectively, and for KCl to examine non-receptor-mediated sensitivity. To reduce venular pressure and flow, vasopressin, which constricts cremaster arterioles but not venules, was applied locally at a maximally effective concentration. This arteriolar constriction had no effect on venular sensitivity to alpha-1-adrenoceptor and KCl-mediated constriction. Venular sensitivity (-log M EC50) to alpha-1 and to KCl activation was 6.20 +/- 0.10 and 1.20 +/- 0.04 in the absence and 6.34 +/- 0.09 and 1.30 +/- 0.03 in the presence of arteriolar constriction, respectively. Venular sensitivity to alpha-2 activation was actually greater during arteriolar constriction (6.25 +/- 0.11 in the absence of constriction versus 7.06 +/- 0.13 in the presence of constriction, p < 0.001). In a second series, the effect of reduced cremaster perfusion pressure and flow on both arteriolar and venular sensitivity was examined by mechanically lowering cremaster inflow. Reduction of first-order arteriolar and venular flow by 82-85% attenuated arteriolar alpha-1 and abolished alpha-2 sensitivity but had no effect on venular adrenergic sensitivity; KCl sensitivity was increased. These data indicate that, in contrast to arteriolar smooth muscle, venular smooth muscle alpha-adrenoceptor sensitivity is preserved during reduced pressure and flow and, thus, is little affected by metabolic and myogenic regulation. The selective depressant effect on arteriolar adrenergic but not KCl constriction suggests that myogenic/metabolic inhibition of arterioles is receptor specific.