Activation of atp-sensitive potassium channels contributes to
reactive hyperemia in humans.
Banitt, Peter F., Paul Smits, Stephen B. Williams, Peter Ganz, Mark A.
Creager.
Vascular Medicine and Atherosclerosis Unit, Cardiovascular
Division, Brigham and Women's Hospital, Harvard Medical School, 75
Francis Street, Boston, Massachusetts, 02115
APStracts 3:0179H, 1996.
Activation of ATP-sensitive potassium (KATP) channels present on
vascular smooth muscle cells causes membrane hyperpolarization and
vasodilation. The purpose of this study was to determine whether KATP
channels contribute to reactive hyperemia in humans. Accordingly, we
studied the effect of tolbutamide, a KATP channel inhibitor, on
reactive hyperemic forearm blood flow. Forearm blood flow was
measured by venous occlusion plethysmography. Forearm ischemia was
produced by inflating a sphygmomanometric cuff on the arm to
suprasystolic pressures for 5 minutes. Following cuff release,
forearm blood flow was measured during the reactive hyperemic phase
for 5 minutes. Tolbutamide (1mM blood concentration, n=6) did not
affect basal (2.4+/-0.2 to 2.2+/-0.1 ml/100ml/min), or peak reactive
hyperemic forearm blood flow (21.9+/-3.8 to 22.6+/-2.9 ml/100ml/min,
each p=ns), but significantly attenuated total hyperemic volume
(12.6+/-1.7 vs. 9.2+/-1.8 ml/100ml, p<0.02). Vehicle (n=6) did
not affect basal flow, peak reactive hyperemic flow or total
hyperemia. To determine whether adenosine or endothelium-derived
nitric oxide contribute to reactive hyperemia via KATP channels,
adenosine (1.5-500_g/min, n=6) and acetylcholine (30_g/min, n=6) were
infused before and during tolbutamide co-infusion. Tolbutamide did
not significantly alter the forearm blood flow response to either
adenosine or acetylcholine. In conclusion, KATP channels contribute
to vasodilation during reactive hyperemia in humans.
Received 21 August 1995; accepted in final form 28 February 1996.
APS Manuscript Number H790-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 May 96