ANTICONSTRICTOR EFFECT OF ENDOTHELIUM SENSITIVITY TO SHEAR-STRESS

The lumen of arterial vessels is controlled by shear stress at the endothelium; increased shear stress relaxes the smooth muscle thus evoking arterial dilatation. Since shear stress relates directly to flow rate and inversely to the third power of the internal diameter, a decrease in diameter at a constant arterial blood flow augments the shear stress which should result in smooth muscle relaxation counteracting the constriction. This anticonstrictor effect must be stronger the higher the arterial blood flow. To demonstrate the effect of endothelium sensitivity to shear stress on arterial constriction we compared constrictions of endothelium-intact femoral arteries of anaesthetized cats at different blood flow rates. An abrupt decrease in transmural pressure from 120 to 90 or 70 mm Hg at almost zero blood flow rate (where the shear stress mechanism is practically inactive) evoked a fast passive decrease in diameter with further progressive constriction. On the other hand, at flow rates of 8-15 ml/min, after passive constriction the artery began to dilate and the resultant constrictor effect appeared to be considerably smaller than in the virtual absence of flow. Analogously, responses to norepinephrine (3 . 10(-7) or 10(-6) M) were smaller the higher the blood flow. The difference in the magnitudes of the responses at different flow rates was precisely equal to the value calculated using the experimental data characterizing the diameter/flow rate relation. Endothelium removal abolished the dependence of the magnitude of the constrictor responses on blood flow. These data suggest that the endothelium sensitivity to shear stress provides considerable inhibition of arterial constrictor responses, whatever the nature of constrictor stimulus.