Effect of subarachnoid hemorrhage on cerebral vasodilatation in response to activation of ATP-sensitive K+ channels in chronically hypertensive rats.
OBJECTIVE
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.
Sobey
C G
CG
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242-1081, USA.
Heistad
D D
DD
Faraci
F M
FM
D018528:ATP-Binding Cassette Transporters; D000818:Animals; D001488:Basilar Artery / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D015640:Ion Channel Gating / Q000187:drug effects; D054086:KATP Channels; D009419:Nerve Tissue Proteins / Q000187:drug effects* / Q000378:metabolism; D010208:Papaverine / Q000494:pharmacology*; D010847:Picolines / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects* / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying; D011714:Pyrans / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology*
D018528:ATP-Binding Cassette Transporters; D054086:KATP Channels; D009419:Nerve Tissue Proteins; D010847:Picolines; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D011714:Pyrans; D014665:Vasodilator Agents; C092520:uK-ATP-1 potassium channel; C061043:aprikalim; D010208:Papaverine; D011188:Potassium