title: Role of K+ATP channels and EDRF in reactive hyperemia in the hindquarters vascular bed of cats.
abstract: The mechanism underlying reactive hyperemia was investigated in the feline hindquarters vascular bed under natural- and constant-flow conditions. A 30-s occlusion of the distal aorta produced a marked hyperemic increase in distal aortic blood flow that was attenuated by the ATP-sensitive K+ (K+ATP) channel blocking agent, glibenclamide. When blood flow to the hindquarters vascular bed was held constant with a pump, interruption of blood flow for 5- to 90-s periods produced reactive vasodilator responses that increased in magnitude and duration as the period of ischemia increased. The magnitude and duration of the reactive vasodilator responses were reduced by K+ATP channel antagonists and an inhibitor of nitric oxide synthase, whereas indomethacin had no significant effect. In the pulmonary vascular bed, under constant-flow, elevated tone conditions, a 30-s period of ischemia produced a small reactive vasodilator response and a larger secondary vasoconstrictor response. The present data suggest that reactive hyperemia in the hindquarters vascular bed is mediated by the opening of K+ATP channels and nitric oxide release and that the reactive hyperemic response is not pronounced in the pulmonary circulation.
authors.affiliation: Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.
authors.forename: R K
authors.initials: RK
authors.lastname: Minkes
authors.forename: J A
authors.initials: JA
authors.lastname: Santiago
authors.forename: T J
authors.initials: TJ
authors.lastname: McMahon
authors.forename: P J
authors.initials: PJ
authors.lastname: Kadowitz
mesh_terms: D000218:Adamantane / Q000031:analogs & derivatives / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002415:Cats; D005905:Glyburide / Q000494:pharmacology; D006614:Hindlimb / Q000098:blood supply*; D006940:Hyperemia / Q000209:etiology / Q000503:physiopathology*; D007511:Ischemia / Q000150:complications / Q000503:physiopathology; D009025:Morpholines / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011652:Pulmonary Circulation / Q000187:drug effects; D012039:Regional Blood Flow / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D009025:Morpholines; D015221:Potassium Channels; D014665:Vasodilator Agents; D009569:Nitric Oxide; C082658:U 37883A; D000255:Adenosine Triphosphate; D001120:Arginine; D019001:Nitric Oxide Synthase; D000218:Adamantane; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester