Arginine vasopressin induces endothelium-dependent vasodilatation of the pulmonary artery. V1-receptor-mediated production of nitric oxide.

Infusion of arginine vasopressin (AVP) decreases pulmonary artery pressure. To determine whether this is due to stimulated release of endothelium-derived relaxing factor in the pulmonary circulation, the authors studied segments of canine pulmonary artery suspended in organ chambers for measurement of isometric force. In segments in which contraction was induced with phenylephrine (10(-6) mol), AVP (10(-12) to 10(-7) mol) produced concentration-dependent relaxation in segments with endothelium but not in segments without endothelium. Greater concentrations of AVP (3 x 10(-7) to 3 x 10(-5) mol) produced comparable contraction in segments with or without endothelium. Endothelium-dependent vasodilation in response to AVP was inhibited by NG-nitro-L-arginine (10(-4) mol) and NG-monomethyl-L-arginine (L-NMMA) (10(-4) mol), inhibitors of nitric oxide synthesis from L-arginine. The inhibitory effect of L-NMMA was attenuated by L-arginine (10(-4) mol). Endothelium-dependent vasodilation in response to AVP was inhibited reversibly by the vasopressin V1-blocker. Arginine vasopressin induces release of endothelium-derived nitric oxide through action on endothelial V1-receptors. Endothelium-derived nitric oxide mediates vasodilatation, which may explain decreased pulmonary resistance during AVP infusion.