Central Injections of Capsaicin Cause Antidiuresis Mediated Through Neurokinin-1 Receptors in Rat Hypothalamus and Vasopressin Release
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概要
- 論文の詳細を見る
Intracerebroventricular injections of capsaicin at 100 - 500 nmol elicited dose-dependent decreases in urine outflow volume in anesthetized, hydrated rats. The capsaicin (500 nmol)-induced anti- diuresis was inhibited by pretreatment with CP96345 (30 nmol, a neurokinin-1-receptor antagonist), but not by that with phenoxybenzamine (20 nmol, an alpha-adrenoceptor antagonist), timolol (100 nmol, a beta-adrenoceptor antagonist) or atropine (300 nmol, a muscarinic antagonist) into the hypothalamic supraoptic nucleus (SON). Intravenous injections of d(CH2)5-D-Tyr(Et)VAVP (50 μg/kg, a vasopressin-receptor antagonist) completely blocked the antidiuresis. In intra-SON microdialysis experiments, acetylcholine concentration in the perfusate of the capsaicin-injected rats was not different from that of the vehicle-injected rats. These findings suggested that capsaicin stimulated substance P release in the SON and caused the antidiuresis as a result of the increased release of vasopressin into the circulation from the neurohypophysis mediated through neurokinin-1 receptors in the SON.
- 社団法人 日本薬理学会の論文
- 1999-02-01
著者
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Mori Mayumi
Department Of Pharmacology Nagoya City University Medical School
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Mori Mayumi
Department Of Hematology Tokyo Metropolitan Geriatric Hospital
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Tsushima Hiromi
Department Of Cellular And Molecular Pharmacology Nagoya City University Graduate School Of Medical
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Mori Mayumi
Department Of Anesthesiology School Of Medicine Fukuoka University
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