Jpn. J. Pharmacol. 79 (2), 237-241 (1999)


Central Injections of Capsaicin Cause Antidiuresis Mediated Through Neurokinin-1 Receptors in Rat Hypothalamus and Vasopressin Release

Hiromi Tsushima and Mayumi Mori


Department of Pharmacology, Nagoya City University Medical School, Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan

Abstract: 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 antidiuresis 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 microg/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.


Keywords: Supraoptic nucleus, Vasopressin, Substance P, Capsaicin, Neurokinin-1 receptor


Copyrightę The Japanese Pharmacological Society 1999

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