Effect of nitric oxide synthase inhibition on arteriovenular control of capillary perfusion

Postcapillary venules contribute to the control of arteriolar tone and therefore capillary perfusion. In a previous study of the rat mesentery, we found a significant correlation between capillary red blood cell velocity (V-RBC) and the percent of the feeding arteriole length that was paired (proximity<15 microns) with a postcapillary venule (% pairing). In the present study using the same model, we test whether nitric oxide (NO) is involved in the arteriovenular control of capillary perfusion. The baseline relationship between VRBc and % pairing (p<0.001; positive slope of 0.079 mm/sec/%) not only is eliminated following NO synthase inhibition with L-NAME, but also becomes negative (p=0.004; -0.035 mm/sec/%). The negative correlation may indicate that in the absence of NO, venules (or venular leukocytes) promote constriction of nearby arterioles, therefore limiting capillary perfusion. For individual capillaries, the decrease in V-RBC (L-NAME minus baseline) was highly correlated with % pairing (p<0.001; r(2)=0.81), with the intercept near zero. This suggests that L-NAME has no effect on capillary perfusion when the arteriolar pathway lacks nearby venules, and that L-NAME has a maximal effect when arteriovenular pairing is high. These results confirm a role for NO in the control of capillary perfusion by arteriovenular communication.