1993 Volume 63 Issue 1 Pages 41-45
It has been reported that there is a continuous release of nitric oxide (NO) that contributes to the regulation of vascular tone in the arterial system. In contrast, the role of NO on vascular tone in the venous system is controversial. We examined the effect of NG-nitro-L-arginine (LNNA), an NO synthase inhibitor, on venous tone in dogs. Venous tone was evaluated by effective vascular stiffness (EVS), which was calculated from the changes in central venous pressure recorded simultaneously with changes in blood volume. LNNA (10 mg/kg, i.v.) increased EVS from 0.21±0.04 to 0.30±0.03 mmHgl kg/ml as well as increasing the systemic vascular resistance. NG-Nitro-D-arginine had no effect on EVS. The LNNA-induced increase in EVS was partly reversed by L-arginine, but not by D-arginine, indicating that the increase in EVS was attributable to a blockade of NO synthesis. Since the present study was conducted under ganglion blockade, nitroxidergic nerve terminals do not seem to be the source of NO in this case. These findings suggest that NO (endothelium-derived relaxing factor) is constantly released in the venous system and contributes to the regulation of total systemic venous tone.