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(Hypertension. 1995;25:1069-1074.)
© 1995 American Heart Association, Inc.

Articles

Cerebral ATP-Sensitive Potassium Channels During Acute Reduction of Carotid Blood Flow

Masato Nishimura; Hakuo Takahashi; Akira Nanbu; Masatoshi Sakamoto; Tadashi Nakanishi; Manabu Yoshimura

From the Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto; and the Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University, Moriguchi City, Osaka (H.T.), Japan.

Correspondence to Masato Nishimura, MD, Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan.

Abstract The ATP-sensitive potassium channels (K_ATP) are activated either by a decrease in intracellular ATP content or by a lowering of the ATP-ADP ratio such as during stroke. We studied the role of cerebral K_ATP on arterial pressure during acute reduction of cerebral blood flow in 12-week-old male Wistar rats anesthetized with urethane by recording arterial pressure and heart rate continuously. After bilateral ligation of the common carotid arteries, glibenclamide, a specific blocker of K_ATP, was injected intracerebroventricularly into the cerebral lateral ventricle. Glibenclamide elicited a sustained vasopressor response in a dose-dependent manner in rats with bilateral carotid artery ligation (10 nmol, +15±2 mm Hg; 1 nmol, +5±1 mm Hg, P<.01 versus vehicle), but hemodynamic alterations were barely recorded with glibenclamide in sham-operated control rats. The abdominal sympathetic discharge was not increased significantly enough to explain the pressor mechanism. Similarly, pretreatments with intravenous injections of bunazosin, an ₁-adrenoceptor antagonist, did not affect the pressor response of intracerebroventricular glibenclamide. To investigate the vasopressor mechanism further, we measured plasma and pituitary concentrations of arginine vasopressin and determined the effects of vasopressin receptor antagonists. The intracerebroventricular injections of glibenclamide significantly increased the plasma concentration of vasopressin (P<.05) and significantly decreased the pituitary concentration of vasopressin (P<.05) in rats with bilateral carotid artery ligation. Intravenous pretreatment with the vasopressin V₁ receptor antagonist OPC-21268 abolished the vasopressor response to intracerebroventricular glibenclamide (+16±2 versus +1±1 mm Hg, P<.01). These findings indicate that K_ATP in the brain may inhibit an excess rise in arterial pressure in part by decreasing the release of vasopressin from the pituitary during bilateral carotid artery ligation.

Key Words: potassium channels • blood pressure • ligation • carotid artery • vasopressin • hypertension, experimental

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