Rk. Minkes et al., ROLE OF K-ATP(+) CHANNELS AND EDRF IN REACTIVE HYPEREMIA IN THE HINDQUARTERS VASCULAR BED OF CATS, American journal of physiology. Heart and circulatory physiology, 38(5), 1995, pp. 1704-1712
The mechanism underlying reactive hyperemia was investigated in the fe
line hindquarters vascular bed under natural- and constant-flow condit
ions. A 30-s occlusion of the distal aorta produced a marked hyperemic
increase in distal aortic blood flow that was attenuated by the ATP-s
ensitive K+ (K-ATP(+)) channel blocking agent; glibenclamide. When blo
od 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 reacti
ve 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-flo
w, elevated tone conditions, a 30-s period of ischemia produced a smal
l reactive vasodilator response and a larger secondary vasoconstrictor
response. The present data suggest that reactive hyperemia in the hin
dquarters 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.