Icv administered epibatidine (EP), a nicotinic receptor (nAChR) agonist, induced secretion of catecholamines (CAs, noradrenaline and adrenaline) from the rat adrenal medulla. Because CAs affect contractility of the bladder and urethra, we examined effects of EP on micturition and their dependence on CAs in urethane-anesthetized (0.8 g/kg, ip) male Wistar rats. Catheters were inserted into the bladder and the femoral artery to perform cystometrograms (CMG) and to collect blood samples, respectively. CMG was started 2 h after the surgery and 1 h after the start, EP (0.3 or 1 nmol) or vehicle was icv administered. Plasma CAs were measured at 5 min after the administration. In some rats, acute bilateral adrenalectomy (ADX) was performed before the insertion. Effects of icv pretreated mecamylamine (MEC, 100 or 300 nmol), a nAChR antagonist, on the EP-induced responses were also examined. Icv administered EP dose-dependently prolonged intercontraction intervals (ICI) and elevated plasma CAs. ADX abolished the EP-induced elevation of both CAs without affecting ICI prolongation. MEC dose-dependently attenuated the EP-induced ICI prolongation and elevation of CAs. These results suggest that activation of brain nAChRs might suppress micturition reflex, which is independent of CAs.