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.
Original language | English (US) |
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Pages (from-to) | H1704-H1712 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 269 |
Issue number | 5 38-5 |
DOIs | |
State | Published - 1995 |
Externally published | Yes |
Keywords
- U- 37883A
- adenosine 5'-triphosphate-sensitive potassium channels
- glibenclamide
- nitric oxide
- peripheral circulation
- pulmonary circulation
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)