Effects of vasopressin on portal-systemic collaterals in portal hypertensive rats: Role of nitric oxide and prostaglandin

This study investigated the effect of vasopressin on portal-systemic collat erals in portal hypertensive rats and the influence of nitric oxide (NO) an d prostaglandin on the responsiveness of collateral vessels to vasopressin. The vascular responsiveness to graded concentrations of vasopressin was te sted with or without the incubation of n(omega)-nitro-L-arginine (NNA) (100 mu mol/L) and/or indomethacin (10 mu mol/L) in perfused collateral vascula r beds of rats with portal hypertension induced by partial portal vein liga tion. In addition, concentration-response curves to vasopressin with incuba tion of a vasopressin V-1 receptor antagonist d(CH2)(5)Tyr(Me) arginine vas opressin and concentration-response curves to a Vt receptor agonist 1-desam ino-8-Darginine vasopressin were performed. Vasopressin significantly incre ased the perfusion pressure of collaterals, and this effect was suppressed by the addition of the V-1 receptor antagonist. Perfusion,vith the V-2 rece ptor agonist had no effect on the collaterals. Incubation with NNA, indomet hacin, or both significantly potentiated the response of collaterals to vas opressin. In addition, the presser response to vasopressin in the combinati on group was significantly higher than that in the NNA-alone group. The res ults show that vasopressin produces a direct vasoconstrictive effect on the portal-systemic collaterals of portal hypertensive rats. This effect is me diated by the vasopressin V-1, but not V-2, receptors. The attenuation of t he response to vasopressin by NO and prostaglandin suggest a function role of both mediators in the regulation of the portal-systemic collateral circu lation in portal hypertensive rats.