Brain carbon monoxide can suppress the rat micturition reflex through brain γ‐aminobutyric acid receptors

Abstract

AbstractObjectivesTo investigate roles of brain carbon monoxide (CO), an endogenous gasotransmitter, in regulation of the rat micturition reflex.MethodsIn urethane‐anesthetized (0.8 g/kg, ip) male rats, evaluation of urodynamic parameters was started 1 h before intracerebroventricular administration of CORM‐3 (CO donor) or ZnPP (non‐selective inhibitor of heme oxygenase, a CO producing enzyme) and continued for 2 h after the administration. We also investigated effects of centrally pretreated SR95531 (GABAA receptor antagonist) or SCH50911 (GABAB receptor antagonist) on the CORM‐3‐induced response.ResultsCORM‐3 significantly prolonged intercontraction intervals (ICIs) without changing maximal voiding pressure (MVP), while ZnPP significantly shortened ICI and reduced single‐voided volume and bladder capacity without affecting MVP, post‐voided residual volume, or voiding efficiency. The ZnPP‐induced ICI shortening was reversed by CORM‐3. The CORM‐3‐induced ICI prolongation was significantly attenuated by centrally pretreated SR95531 or SCH50911, respectively.ConclusionsBrain CO can suppress the rat micturition reflex through brain γ‐aminobutyric acid (GABA) receptors.