Decreased mesenteric vascular response to angiotensin II in portal hypertension.

We studied the mesenteric and systemic vascular response to angiotensin II in normotensive and portal hypertensive (PHT) rabbits, because of the documented poor tolerance of hemorrhagic shock in PHT. Normally, the hemodynamic response to angiotensin II (AII) is characterized by selective and disproportionate splanchnic vasoconstriction. We postulated that the response to AII could be diminished in PHT. Chronic PHT was induced by partial portal vein ligation 3 weeks prior to graded angiotensin II infusion. Baseline hemodynamic measurements showed markedly elevated portal pressure (PPV) and superior mesenteric artery blood flow (QSMA) compared with those of normotensive animals (P less than 0.01). Superior mesenteric artery resistance (RSMA) was markedly reduced in PHT compared to that in controls (P less than 0.05). Angiotensin II infusion in normals resulted in a marked selective rise in RSMA compared with the rise in systemic resistance (RSYS) (P less than 0.01). AII infusion in PHT resulted in a rise in RSMA and RSYS, but the disproportionate in RSMA was attenuated. Furthermore, in both normal and PHT, AII caused a significant rise in PPV (P less than 0.01). We conclude that the findings indicate that the splanchnic vasoconstrictive response to AII is substantially impaired in PHT, and that AII will paradoxically cause a rise in PPV, possibly aggravating the tendency to hemorrhage in PHT.