Hypertension, Vol 22, 677-681, Copyright © 1993 by American Heart Association
T Kitazono, DD Heistad and FM Faraci
We examined the hypothesis that dilatation of the basilar artery in
response to activation of ATP-sensitive potassium channels is impaired in
stroke-prone spontaneously hypertensive rats (SHRSP). Changes in basilar
artery diameter in response to aprikalim, a direct activator of
ATP-sensitive potassium channels, were measured in anesthetized SHRSP and
normotensive Wistar-Kyoto (WKY) rats through a cranial window. Topical
application of aprikalim increased basilar artery diameter in WKY rats.
Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels,
abolished aprikalim-induced vasodilatation. Thus, ATP-sensitive potassium
channels are functional in the basilar artery of WKY rats in vivo.
Aprikalim (10(-6) mol/L) dilated the basilar artery by 31 +/- 5% (mean +/-
SEM) in WKY rats but only 5 +/- 1% in SHRSP. The concentration-response
curve to aprikalim in SHRSP was significantly shifted to the right, but the
response to the highest concentration of aprikalim (10(-5.5) mol/L) was
similar in SHRSP and WKY rats. Vasodilatation in response to norepinephrine
was also impaired in SHRSP. Dilator responses of the basilar artery to
forskolin, a direct activator of adenylate cyclase, and nitroprusside, a
direct activator of guanylate cyclase, were normal in SHRSP. The findings
suggest that dilatation of the basilar artery in response to direct
activation of ATP-sensitive potassium channels is impaired in SHRSP
compared with WKY rats in vivo.
ARTICLES
ATP-sensitive potassium channels in the basilar artery during chronic hypertension
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
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