Role of k+atp channels and endothelium-derived relaxing factor in
reactive hyperemia in the hindquarters vascular bed of the cat.
Minkes, Robert K., Jos[acute]e A. Santiago, Timothy J. McMahon, and
Philip J. Kadowitz.
Department of Pharmacology, Tulane University School of Medicine,
New Orleans, LA 70112
APStracts 2:0169H, 1995.
The mechanism underlying reactive hyperemia was investigated in the
feline hindquarters vascular bed under natural and constant flow
conditions. A 30-sec occlusion of the distal aorta produced a marked
hyperemic increase in distal aortic blood flow that was attenuated by
the K+ATP channel blocking agent, glybenclamide. When blood flow to
the hindquarters vascular bed was held constant with a pump,
interruption of blood flow for 5-90 sec 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-sec 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.
Received 27 February 1995; accepted in final form 4 April 1995.
APS Manuscript Number H186-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.