Renal preservation resistance: evidence against myogenic vasoactive factors.
Vasoconstriction is believed to be a dominant cause of high perfusion resistance during kidney preservation at low temperatures. An experiment was performed to study the effects of hypothermia on vasoactivity. Measurements were made on an apparatus that permitted perfusion resistance to be compared simultaneously in two isolated kidneys at different temperatures. With perfusion temperature serving as the variable, the vascular responses to several vasoactive agents were measured. Hypothermia diminished or altered the vascular responses to the agents. For example, no vasoconstriction was observed with Angiotensin II, dopamine, acetylcholine, or BaCl2 and no vasodilation was observed with papaverine or bradykinin in the hypothermic kidney. A significantly altered response was observed with norepinephrine. The responses were reversible upon return to normothermia. From these data, we conclude that myogenic vasoconstriction plays a questionable role in producing the elevated perfusion resistance observed in some hypothermic kidneys.
D000109:Acetylcholine / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D001920:Bradykinin / Q000494:pharmacology; D003080:Cold Temperature; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D007668:Kidney / Q000098:blood supply*; D009638:Norepinephrine / Q000494:pharmacology*; D009926:Organ Preservation; D010208:Papaverine / Q000494:pharmacology; D010477:Perfusion; D014666:Vasomotor System / Q000187:drug effects*
D000804:Angiotensin II; D001464:Barium; D010208:Papaverine; D000109:Acetylcholine; D001920:Bradykinin; D004298:Dopamine; D009638:Norepinephrine