ATP-sensitive potassium channels in the basilar artery during chronic hypertension

Takanari Kitazono, Donald D. Heistad, Frank M. Faraci

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)677-681
Number of pages5
JournalHypertension
Volume22
Issue number5
DOIs
Publication statusPublished - Nov 1993

All Science Journal Classification (ASJC) codes

  • Internal Medicine

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