ROLE OF VENULAR ENDOTHELIUM IN CONTROL OF ARTERIOLAR DIAMETER DURING FUNCTIONAL HYPEREMIA

This study was designed to determine the importance of the venular end othelium in the vasodilation of adjacent arterioles during functional hyperemia. The hamster cremaster muscle was prepared for in vivo micro scopy. Two silver-silver chloride electrodes were placed across the pe dicle of the cremaster muscle, and a square-wave pulse (10 V amplitude , 1 ms duration, and 1 Hz frequency) was used to elicit muscle contrac tion. Muscle stimulation for 1 min resulted in a vasodilation of the f irst-order arterioles from 74 +/- 2 to 91 +/- 2 mu m (n = 9, P < 0.05) . After perfusion of the venule with air to disrupt the venular endoth elium, there was no significant effect on the resting diameter, 73 +/- 3 mu m, but the vasodilation associated with the muscle stimulation w as significantly attenuated to 82 +/- 3 mu m (P < 0.01). After complet ion of these experiments, the disruption of venular endothelium was co nfirmed by electron microscopy. The functional vasodilation of arterio les adjacent to venules with an intact endothelium (venules in which a ir did not enter) was retained after air perfusion (n = 6). These resu lts suggest that the presence of the venular endothelium is important for the arteriolar vasodilation during functional hyperemia. We propos e that the venular endothelium releases a relaxing factor responsible for a portion of the functional arteriolar vasodilation.