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Abstract
Objective Arginine vasopressin (AVP) exerts a constrictive effect on the portal-systemic collaterals of non-cirrhotic portal hypertensive rats, but its effect on cirrhotic rats is unknown. The aim of this study was to investigate the response of AVP and the modulatory roles of nitric oxide and prostaglandin on collaterals of common bile duct-ligated (BDL) cirrhotic rats. Material and methods The collateral vascular responsiveness to graded concentrations of AVP (10−10–3×10−7 M) was tested by an in situ collateral perfusion system pretreated with Nω-nitro-L-arginine (L-NNA, 100 μM), indomethacin (INDO, 10 μM), or both. The collateral responses to AVP with the pretreatment of a vasopressin V1 receptor antagonist d(CH2)5Tyr(Me) arginine vasopressin or a V2 receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP, 10−10–3×10−7 M) were also evaluated. Results The perfusion pressure of collaterals was significantly increased by AVP, and this effect was inhibited by the addition of the V1 receptor antagonist. DDAVP had no effect on the collaterals. Incubation with L-NNA or L-NNA plus INDO, but not INDO alone, significantly potentiated the constrictive effects of AVP. The constrictive effect of AVP in the combination group was similar to that in the L-NNA alone group. Conclusions The results show that AVP produces a direct vasoconstrictive effect on the portal-systemic collaterals of BDL cirrhotic rats. The constrictive effect of AVP is mediated by the vasopressin V1, instead of V2, receptors. Nitric oxide may play a more important role than prostaglandin in modulating the collateral vascular response to AVP in BDL cirrhotic rats.