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


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.

Duke Authors

Cited Authors

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

Published Date

  • December 15, 1995

Published In

Volume / Issue

  • 269 / 5 38-5

International Standard Serial Number (ISSN)

  • 0363-6135

Citation Source

  • Scopus