Introduction: Obstructive cholestasis is clinically characterized clinically by jaundice, discolored urine, pale stools, pruritus, liver cirrhosis and portal hypertension, causing a high rate of morbidity and mortality in human clinical area. Microsurgical extrahepatic cholestasis (MHC) is the most commonly used model to study obstructive cholestasis since it presents with a systemic inflammatory response syndrome, characterized by hyperdynamic circulation, peripheral sympathetic hyperactivity and multiorgan dysfunction. The aim of the present study was to analyse the possible alterations on vascular function produced by microsurgical extrahepatic cholestasis. Methods: Cholestasis induction was made under anaesthesia (ketamine/xylacine) by a surgical operation based on the ligation of the common bile duct and the 4 bile ducts and then the cut of them. Contraction to phenylephrine (Phe) was measured in MRA from SO (sham-operated) and MHC (maintained for 7-8 weeks) rats. Participation of nitric oxide (NO) and thromboxane A2 (TxA2) in this response was determined, as well as the vasomotor responses to exogenous NO and TXA2. Results: MHC decreased vasoconstrictor response to Phe in MRA from MHC rats. Preincubation with NO synthesis inhibitor L-NAME increased the Phe-induced contraction in a similar extent in both groups. Preincubation with the COX-1/2 or COX-2 inhibitor (indomethacin and NS-398, respectively), decreased the Phe-induced contraction only in SO animals. TXA2 synthesis inhibitor (furegrelate) also decreased Phe contraction only in SO animals. Vasomotor responses to DEA-NO (NO donor) or U-46619 (TXA2 analog) were not modified by MHC. Conclusion: MHC decreases Phe-induced vasoconstriction in MRA. This decrease is due to a decrease on contractile prostanoid participation in this response, probably through a decrease on TXA2 release, while the participation of NO on this modification is ruled out.