Abstract
Purpose: This study was performed to assess the effect of L-type voltage-dependent calcium channel (VDCC) blocker (dilitiazem) on the response of the urinary bladder with ethanol intoxication in in vivo and in vitro studies. Materials and Methods: Sprague-Dawley rats were used for in vivo and in vitro studies. The strips were divided into 5 groups according to pretreatment. Group I-A was treated with ethanol (0.1%), group I-B with ethanol (0.5%), group II with diltiazem treatment (10–6M), group III-A with pretreatment of diltiazem (10–6M) with ethanol intoxication (0.1%) and group III-B with pretreatment of diltiazem with ethanol intoxication (0.5%). The carbachol-induced tension was compared before and after each pretreatment. In separate in vivo experiments, the changes of maximal vesical pressure and intercontraction interval after intra-arterial administration of each agent (identical grouping with in vitro study) were monitored. Results: The carbachol-induced contractions in group I-A, group I-B, group II, group III-A and group III-B were significantly decreased after each pretreatment (95 ± 2.73%, 92.6 ± 2.5%, 65.4 ± 2.0%, 52.61 ± 5.16%, 14.9 ± 1.4% of the control). The degree of increment of intercontraction interval and decrement of maximal vesical pressure showed a significant difference in the presence of diltiazem and ethanol intoxication (0.5%) compared with the diltiazem-treated and ethanol-intoxicated groups (0.5%). Conclusions: There is a possibility that ethanol and L-type VDCC blockers have synergistic depressive effect on bladder contractility and that ethanol and L-type VDCC blockers act through a common ionic pathway.