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 V_RBC 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 VRBC (L-NAME minus baseline) was highly correlated with % pairing (p<0.001; r²=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.