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Am J Physiol Regul Integr Comp Physiol (April 10, 2003). doi:10.1152/ajpregu.00109.2003
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Submitted on March 6, 2003
Accepted on April 4, 2003

Effect of (±)-epibatidine, a nicotinic agonist, on the central pathways controlling voiding function in the rat

Sun-Ju Lee1*, Yasuo Nakamura2, and William C de Groat3

1 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Urology, Kyung Hee University College of Medicine, Seoul, Korea
2 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Urology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, Japan
3 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

* To whom correspondence should be addressed. E-mail: sjlee{at}khu.ac.kr.

Nicotinic receptors in the brain modulate the release of many transmitters that are known to regulate voiding. This prompted us to examine the central nervous system effects of a neuronal nicotinic agonist, (±)-epibatidine, on voiding function in awake and anesthetized rats. Intracerebroventricular (i.c.v.) injection of (±)-epibatidine (0.1 µg) significantly increased intercontraction interval (ICI), but did not change pressure threshold (PT), or maximal voiding pressure (MVP); whereas 1 µg of (±)-epibatidine increased PT, MVP (P<0.05) and decreased ICI. A low i.v. dose of (±)-epibatidine (0.001-0.1 µg) had no effect; however, a large dose of (±)-epibatidine (1 µg) significantly decreased ICI and increased MVP (P<0.05) but did not change PT (P>0.05). The effects occurred within 5-10 min after injection and persisted for 1-2 h. I.c.v. chlorisondamine (10 µg), a nicotinic receptor antagonist, blocked the effect of i.c.v. (±)-epibatidine (0.1 µg). The experiments revealed that activation of nicotinic receptors in the brain increased bladder capacity in awake and anesthetized rats. These results suggest that the nicotinic agonist can activate mechanism that inhibit voiding reflexes.




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