The effect of hypoxia on angiotensin-stimulated release of PGI2 from the splanchnic bed.

The effect of hypoxia on splanchnic angiotensin II (AII)-stimulated prostaglandin (PG) release was examined in male rats. The superior mesenteric artery was cannulated and perfused in vitro with physiologic buffer at a pO2 of 460 or 60 torr. Splanchnic vessels were perfused isolated (SV) or in continuity with the small intestine (SV + SI). AII (10-300 ng) was infused as bolus injections. Quantitative analysis of SV + SI effluent by bioassay indicated the predominant PG released was PGI2. Quantitative analysis by radioimmunoassay confirmed PGI2 as the major PG released from the SV and SV + SI following AII stimulation. Relative hypoxia significantly decreased AII-stimulated release of PGI2 from the SV, and only modestly from the SV + SI. These data demonstrate two splanchnic sources of AII-stimulated vasodilator PG synthesis, the SV and SV + SI, with the SV more sensitive to relative hypoxia. Diminished release of splanchnic vascular (SV) vasodilator PGI2 may be of importance in AII-mediated splanchnic vasoconstriction seen in hypoxia and shock.