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.
Reed
M
M
David Grant U.S. Air Force Medical Center, Travis Air Force Base, California.
Taylor
B
B
Myers
S I
SI
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001681:Biological Assay; D015232:Dinoprostone / Q000096:biosynthesis; D011464:Epoprostenol / Q000096:biosynthesis*; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000502:physiology*; D009130:Muscle, Smooth / Q000378:metabolism; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains; D013928:Thromboxane A2 / Q000096:biosynthesis
D000804:Angiotensin II; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D015232:Dinoprostone