Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent

Background: Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model. Methods: Ang II was infused in incremental doses (0-200 μg · h⁻¹) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (P_SMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (P_tiO₂) and lactate fluxes. Results: Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (R_SMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased R_SMA only minimally when P_SMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased P_tiO₂ at a P_SMA of 50 mmHg, splanchnic lactate production was not observed. Conclusion: We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure.