CEREBRAL ADENOSINE TRIPHOSPHATE-SENSITIVE K-ISCHEMIA IN SPONTANEOUSLYHYPERTENSIVE RATS( CHANNELS MAY BE IMPAIRED DURING ACUTE CEREBRAL)

To elucidate the role of cerebral adenosine triphosphate (ATP)-sensiti ve K+ channels (K-ATP) on arterial pressure regulation during acute ce rebral ischemia in spontaneously hypertensive rats (SHR), intracerebro ventricular (i.c.v.) injections of either glibenclamide, a specific bl ocker of K-ATP or pinacidil, a K-ATP opener, were performed in SHR and Wistar-Kyoto rats (WKY). Intracerebroventricular injections of gliben clamide elicited a vasopressor response in WKY with bilateral ligation of the carotid arteries, whereas the response was smaller in SHR. It increased plasma AVP, but decreased pituitary AVP in WKY with ligation , but not in SHR. Systemic administration of an AVP V-1 receptor antag onist, OPC-21268, abolished the vasopressor responses to i.c.v. inject ions of glibenclamide in WKY. Bilateral ligation of the carotid arteri es augmented the vasodepressor responses to i.c.v. injections of pinac idil in WKY, but not in SHR. Cerebral K-ATP may play a role in bufferi ng a rise in arterial pressure by inhibiting the release of AVP from t he pituitary glands during acute cerebral ischemia in WKY, but this me chanism might be deranged in SHR, probably due to impaired responsiven ess of cerebral K-ATP to ischemia.