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

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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 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(CH<SUB>2</SUB>)<SUB>5</SUB>-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.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 79(2), 237-241, 1999-02-01

    The Japanese Pharmacological Society

References:  23

Codes

  • NII Article ID (NAID)
    10008682503
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    REV
  • ISSN
    00215198
  • NDL Article ID
    4663616
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  NDL  J-STAGE 
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