Role of K+ATP channels and EDRF in reactive hyperemia in the hindquarters vascular bed of cats.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Minkes, RK; Santiago, JA; McMahon, TJ; Kadowitz, PJ

Published Date

  • November 1995

Published In

Volume / Issue

  • 269 / 5 Pt 2

Start / End Page

  • H1704 - H1712

PubMed ID

  • 7503268

International Standard Serial Number (ISSN)

  • 0002-9513

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.1995.269.5.H1704


  • eng

Conference Location

  • United States