Influence of Venular Prostaglandin Release on Arteriolar Diameter During Functional Hyperemia

Abstract

Indomethacin treatment or removal of the venular endothelium will attenuate functional arteriolar vasodilation in the hamster cremaster muscle. We tested the hypothesis that prostanoid release from venular endothelial cells was responsible for the functional vasodilation of the paired arteriole. The hamster cremaster muscle was prepared for in vivo microscopy and stimulated for 1 minute (10V, 40 μsec, 1 Hz). Before a second muscle stimulation, the venular endothelium was removed by perfusing the venule with several air bubbles. A third muscle stimulation was performed during prostaglandin inhibition (28 μmol/L indomethacin superfusion). Arterioles (n=9, 55±5 μm) dilated 25±4% during the initial muscle stimulation. After removal of the endothelium from the paired venules, there was no effect on resting arteriolar diameters (53±4 μm), but the functional arteriolar dilation was attenuated to 15±5% ( P <.05). The additional indomethacin treatment had a significant effect on resting diameter (50±4 μm) but did not alter the magnitude of the functional vasodilation (11±4%, P >.05). In a second set of experiments, the order of the experimental protocol was reversed. Muscle stimulation resulted in a 23±2% increase in diameter (47±2 to 57±2 μm). Indomethacin treatment significantly attenuated the functional dilation to 8±3% (45±2 to 48±2 μm). Arteriolar diameter was significantly smaller after disruption of the venular endothelium with air bubbles (40±2 μm), but there was no effect on the functional vasodilation, 8±3% increase in diameter (to 43±2 μm). These results suggest that the arteriolar dilatory response to muscle stimulation is mediated, in part, by prostanoid release from the venular endothelium.