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(Stroke. 1997;28:392-397.)
© 1997 American Heart Association, Inc.

Articles

Effect of Subarachnoid Hemorrhage on Cerebral Vasodilatation in Response to Activation of ATP-Sensitive K⁺ Channels in Chronically Hypertensive Rats

Christopher G. Sobey, PhD; Donald D. Heistad, MD Frank M. Faraci, PhD

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.

Correspondence to Dr Donald Heistad, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242-1081.

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 cisterna magna.

Results Under control conditions, aprikalim (0.1 to 1 µmol/L) and papaverine (10 to 100 µmol/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.

Editorial Comment

David R. Harder, PhD, Guest Editor

Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wis

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