M Saito1, A Kondo. 1. Department of Urology, Nagoya University School of Medicine, Japan.
Abstract
BACKGROUND: Overactivity of the detrusor due to benign prostatic hyperplasia may be induced by hyperpermeability of the smooth muscle cell membrane to calcium. We investigated the effect of verapamil, a calcium channel blocker, on detrusor function in outflow obstructed and control rat bladders. METHODS: Verapamil was injected intravenously via a catheter inserted into the internal jugular vein in doses of 0.5, 1.0, 2.0, 4.0, and 10.0 mg/kg in rat bladders with and without partial outflow obstruction under urethane anaesthesia. The intravesical pressure was monitored continuously. We measured the tidal voided urine volume, the voiding pressure, the pressure at which micturition was induced, and the end-point pressure of micturition. RESULTS: The tidal voided urine volume was significantly decreased in the obstructed bladders before administration of verapamil. Verapamil had similar effects in cystometric parameters in obstructed and control bladders. Verapamil increased the tidal voided urine volume, the pressure at which micturition was induced, and the end-point pressure of micturition, and reduced the voiding in obstructed and control bladders. Verapamil at doses of 4.0 mg/kg or higher induced significant arrhythmia. CONCLUSIONS: Verapamil reduced the contractile force of the bladder and increased the capacity and residual urine volume in both normal and obstructed bladders. Thus, although calcium channel blockers such as verapamil may be effective in treating a hyperactive bladder, they may have adverse cardiovascular effects.
BACKGROUND: Overactivity of the detrusor due to benign prostatic hyperplasia may be induced by hyperpermeability of the smooth muscle cell membrane to calcium. We investigated the effect of verapamil, a calcium channel blocker, on detrusor function in outflow obstructed and control rat bladders. METHODS:Verapamil was injected intravenously via a catheter inserted into the internal jugular vein in doses of 0.5, 1.0, 2.0, 4.0, and 10.0 mg/kg in rat bladders with and without partial outflow obstruction under urethane anaesthesia. The intravesical pressure was monitored continuously. We measured the tidal voided urine volume, the voiding pressure, the pressure at which micturition was induced, and the end-point pressure of micturition. RESULTS: The tidal voided urine volume was significantly decreased in the obstructed bladders before administration of verapamil. Verapamil had similar effects in cystometric parameters in obstructed and control bladders. Verapamil increased the tidal voided urine volume, the pressure at which micturition was induced, and the end-point pressure of micturition, and reduced the voiding in obstructed and control bladders. Verapamil at doses of 4.0 mg/kg or higher induced significant arrhythmia. CONCLUSIONS:Verapamil reduced the contractile force of the bladder and increased the capacity and residual urine volume in both normal and obstructed bladders. Thus, although calcium channel blockers such as verapamil may be effective in treating a hyperactive bladder, they may have adverse cardiovascular effects.