ROLE OF K-ATP(+) CHANNELS AND EDRF IN REACTIVE HYPEREMIA IN THE HINDQUARTERS VASCULAR BED OF CATS

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.