Journal article
Functional activity of Ca2+-dependent K+ channels is increased in basilar artery during chronic hypertension
American journal of physiology. Heart and circulatory physiology, Vol.272(3), pp.H1287-H1291
03/01/1997
DOI: 10.1152/ajpheart.1997.272.3.H1287
PMID: 9087603
Abstract
We examined the hypothesis that activity of Ca2+-dependent K+ 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 +/- SE) 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 Ca2+-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 Ca2+-dependent K+ channels. In contrast to constrictor responses to TEA and iberiotoxin, constrictor responses of the basilar artery in response to serotonin and U-46619 were similar in WKY and SHRSP. In WKY rats that were made chronically hypertensive (arterial pressure = 172 +/- 6 mmHg) after treatment for 4 wk with N(G)-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 Ca2+-dependent K+ channels is enhanced in the basilar artery in vivo in two models of chronic hypertension. Thus Ca2+-dependent K+ channels in the basilar artery may be activated during chronic hypertension, perhaps as a response to elevation of intracellular concentration of Ca2+.
Details
- Title: Subtitle
- Functional activity of Ca2+-dependent K+ channels is increased in basilar artery during chronic hypertension
- Creators
- Roberto Paterno - Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City 52242, USADonald D Heistad - Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City 52242, USAFrank M Faraci - Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City 52242, USA
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.272(3), pp.H1287-H1291
- DOI
- 10.1152/ajpheart.1997.272.3.H1287
- PMID
- 9087603
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 03/01/1997
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040583602771
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