Journal article
Effect of nitric oxide and potassium channel agonists and inhibitors on basilar artery diameter
American journal of physiology. Heart and circulatory physiology, Vol.272(1), pp.H256-H262
01/01/1997
DOI: 10.1152/ajpheart.1997.272.1.H256
PMID: 9038945
Abstract
The first goal of this study was to examine the hypothesis that dilatation of the basilar artery in response to activation of ATP-sensitive K+ channels is mediated by nitric oxide (NO). Diameter of the basilar artery (209 +/- 5 microns, mean +/- SE) was measured using a cranial window in anesthetized rats. Aprikalim (a direct activator of ATP-sensitive K+ channels) dilated the basilar artery under control conditions. Inhibition of endogenous NO production with NG-nitro-L-arginine (L-NNA, 10(-4) M) did not alter responses to aprikalim. The second goal was to determine whether vasodilatation in response to NO is dependent on activation of calcium-activated K+ channels. Tetraethylammonium (TEA, 10(-3) M), an inhibitor of calcium-activated K+ channels, did not affect dilator responses to sodium nitroprusside (an NO donor) under control conditions. Responses to nitroprusside (10(-8) and 10(-7) M) were augmented more than twofold during application of L-NNA. In the presence of L-NNA, the augmented portion of the response to nitroprusside was inhibited by TEA and iberiotoxin (5 x 10(-8) M, a highly selective inhibitor of calcium-activated K+ channels), but it was not inhibited by glibenclamide (10(-6) M), an inhibitor of ATP-sensitive K+ channels. These findings suggest that dilator responses of the basilar artery to an activator of ATP-sensitive potassium channels are not mediated by NO. Calcium-activated K+ channels may not normally contribute to dilator responses of the basilar artery to nitroprusside. The effects of TEA and iberiotoxin suggest that when endogenous production of NO is inhibited, sodium nitroprusside causes the opening of calcium-activated K+ channels, contributing to an augmented vasodilator response.
Details
- Title: Subtitle
- Effect of nitric oxide and potassium channel agonists and inhibitors on basilar artery diameter
- Creators
- C. G Sobey - Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USAF. M Faraci - Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.272(1), pp.H256-H262
- DOI
- 10.1152/ajpheart.1997.272.1.H256
- PMID
- 9038945
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 01/01/1997
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040560602771
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