Journal article
Effect of Subarachnoid Hemorrhage on Cerebral Vasodilatation in Response to Activation of ATP-Sensitive K+Channels in Chronically Hypertensive Rats
Stroke (1970), Vol.28(2), pp.392-397
02/1997
DOI: 10.1161/01.STR.28.2.392
PMID: 9040696
Abstract
Background and purpose: Cerebral vasodilatation in response to aprikalim, an opener of ATP-sensitive K+ channels, is selectively augmented after subarachnoid hemorrhage (SAH). Vasodilatation in response to activation of ATP-sensitive K+ channels, however, is impaired during chronic hypertension. Hypertension may contribute to a worse outcome after SAH, but the nature of the relationship between hypertension and SAH is uncertain. In the present study we examined responses of the basilar artery to aprikalim after SAH in normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP).
Methods: In anesthetized WKY and SHRSP, we measured changes in diameter of the basilar artery in response to aprikalim and papaverine using a cranial window 2 days after injection of 0.3 mL saline or autologous blood into the cistema magna.
Results: Under control conditions, aprikalim (0.1 to 1 mumol/L) and papaverine (10 to 100 mumol/L) produced dilatation of the basilar artery. After SAH, responses to aprikalim were not significantly altered in WKY and were markedly increased in SHRSP compared with saline-injected control rats. In contrast, vasodilator responses to papaverine were not changed by SAH in either WKY or SHRSP, suggesting that augmented vasodilatation in response to aprikalim after SAH was selective.
Conclusions: Responses of the basilar artery to aprikalim were greatly augmented in SHRSP after SAH. Because vasodilator responses to many stimuli are impaired after SAH and cerebral vasodilator responses to several stimuli are impaired by chronic hypertension, augmented responses to activation of K+ channels despite the presence of hypertension are unusual.
Details
- Title: Subtitle
- Effect of Subarachnoid Hemorrhage on Cerebral Vasodilatation in Response to Activation of ATP-Sensitive K+Channels in Chronically Hypertensive Rats
- Creators
- Christopher G Sobey - the Departments of Internal Medicine (C.G.S., D.D.H., F.M.F.) and Pharmacology (D.D.H., F.M.F.), Cardiovascular Research Center, and Center on Aging, University of Iowa College of Medicine, Iowa CityDonald D Heistad - the Departments of Internal Medicine (C.G.S., D.D.H., F.M.F.) and Pharmacology (D.D.H., F.M.F.), Cardiovascular Research Center, and Center on Aging, University of Iowa College of Medicine, Iowa CityFrank M Faraci - the Departments of Internal Medicine (C.G.S., D.D.H., F.M.F.) and Pharmacology (D.D.H., F.M.F.), Cardiovascular Research Center, and Center on Aging, University of Iowa College of Medicine, Iowa City
- Resource Type
- Journal article
- Publication Details
- Stroke (1970), Vol.28(2), pp.392-397
- DOI
- 10.1161/01.STR.28.2.392
- PMID
- 9040696
- ISSN
- 0039-2499
- eISSN
- 1524-4628
- Language
- English
- Date published
- 02/1997
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040242002771
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