Inhibition of vascular ATP-sensitive K+ channels does not affect reactive hyperemia
in human forearm.
Farouque, H. M. Omar and Ian T. Meredith.
Cardiovascular Research Centre, Monash Medical Centre and Monash University,
Melbourne, Victoria, 3168, Australia.
APStracts 9:0494H, 2002.
The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in
humans is unresolved. We examined the role of ATP-sensitive K+ channels in regulating
reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects
had forearm blood flow measured with venous occlusion plethysmography. Reactive
hyperemia could be reproducibly induced (n = 9). The contribution of vascular ATP-
sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood
flow before and during brachial artery infusion of glibenclamide lyophilisate, a ATP-
sensitive K+ channel inhibitor (n = 12). To document ATP-sensitive K+ channel
inhibition with glibenclamide lyophilisate, coinfusion with diazoxide, a ATP-sensitive
K+ channel opener, was undertaken (n = 10). Glibenclamide lyophilisate did not
significantly alter resting forearm blood flow or the initial and sustained phases of
reactive hyperemia. However, glibenclamide lyophilisate attenuated the hyperemic
response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do
not play an important role in controlling forearm reactive hyperemia, and that other
mechanisms are active in this adaptive response.
Received 8 April 2002; accepted in final form 23 October 2002
APS Manuscript Number H315-2.
Article publication pending Am J Physiol Heart Circ Physiol
ISSN 1080-4757 Copyright 2002 The American Physiological Society.
Published in APStracts on 25 November 2002