Functional activity of calcium-dependent potassium channels is
increased in the basilar artery in vivo during chronic
hypertension.
Patern, Roberto, Donald D. Heistad, and Frank M. Faraci.
Departments of Internal Medicine and Pharmacology, Cardiovascular
Center and Center on Aging, University of Iowa College of Medicine,
Iowa City, Iowa 52242, USA
APStracts 3:0419H, 1996.
We examined the hypothesis that activity of Ca++-dependent potassium
channels is increased in the basilar artery during chronic
hypertension. Diameter of the basilar artery was measured using a
cranial window in anesthetized normotensive Wistar-Kyoto rats (WKY,
arterial pressure = 109 3 mmHg) (mean SEM) and stroke-prone
spontaneously hypertensive rats (SHRSP, arterial pressure = 179 4
mmHg). Responses of the basilar artery to topical application of
tetraethylammonium ion (TEA), an inhibitor of Ca++-dependent K+
channels, were examined in WKY and SHRSP. Vessel diameter decreased
by 2 1 and 4 0.1% in WKY and by 7 2 and 18 1% in SHRSP (P<0.05
vs WKY) in response to 10-4 and 10-3 M TEA, respectively. Similar
results were obtained using iberiotoxin (10-8 and 10-7 M), a highly
selective inhibitor of Ca++- dependent K+ channels. In contrast to
constrictor responses to TEA and iberiotoxin, constrictor responses
of the basilar artery in response to serotonin and U46619 were
similar in WKY and SHRSP. In WKY rats which were made chronically
hypertensive (arterial pressure = 172 6 mmHg) following treatment for
four weeks with NG-nitro-L-arginine methyl ester, an inhibitor of
nitric oxide synthase, constriction of the basilar artery in response
to TEA was also enhanced. These findings suggest that activity of
Ca++-dependent K+ channels is enhanced in the basilar artery in vivo
in two models of chronic hypertension. Thus, Ca++-dependent K+
channels in the basilar artery may be activated during chronic
hypertension, perhaps as a response to elevation of intracellular
concentration of Ca++.
Received 19 January 1996; accepted in final form 11 September
1996.
APS Manuscript Number H43-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996