Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

Pregnancy produces marked systemic vasodilation, but the mechanism is unkno wn. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased va scular conductance, but that the contribution varies among vascular beds. R abbits were instrumented with aortic and vena caval catheters and ultrasoni c flow probes implanted around the ascending aorta, superior mesenteric art ery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intr avenous injection of N-omega-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first befo re pregnancy (NP) and then at the end of gestation (P). L-NA produced simil ar increases in arterial pressure between groups, but the following respons es were larger (P<0.05) when the rabbits were pregnant: 1) decreases in tot al peripheral conductance [-3.7<plus/minus>0.3 (NP), -5.0 +/-0.5 (P) ml.min (-1).mmHg(-1)], (2)) decreases in mesenteric conductance [-0.47 +/-0.05 (NP ), -0.63 +/-0.07 (P) ml.min(-1).mmHg(-1)], 3) decreases in terminal aortic conductance [-0.43 +/-0.05 (NP), -0.95 +/-0.19 ml.min(-1).mmHg(-1) (P)], an d 4) decreases in heart rate [-41 +/-4 (NP), -62 +/-5 beats/min (P)]. Never theless, total peripheral and terminal aortic conductances remained elevate d in the pregnant rabbits (P<0.05) after L-NA. Furthermore, decreases in ca rdiac output and femoral conductance were not different between the reprodu ctive states. We conclude that the contribution of NO to vascular tone incr eases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate . Finally, unknown factors in addition to NO must also underlie the basal v asodilation observed during pregnancy.