The Effect of Diabetes Mellitus on α1-Adrenergic Receptor Subtypes in the Bladder of Rats

OBJECTIVE To detect the possible alterations on density or sensitivity of alpha 1-adrenergic subtypes in diabetic bladder by reverse transcriptase-polymerase chain reaction technology and in vitro studies. METHODS Experimental diabetes was induced by administration of streptozotocin with a single injection through the tail vein. Rats were divided into control and diabetic groups. Contractile responses of bladder strips from each group were obtained for postassium chloride, adenosine triphosphate, and electrical field stimulation (0.5-32 Hz) in organ bath. Electrical field stimulation responses of strips were evaluated in the presence of PPADS (nonselective P2 antagonist), atropine (cholinergic antagonist), 5 MU (alpha-1a-adrenergic antagonist), BMY-7378 (alpha-1d-adrenergic antagonist), and finally CED (alpha-1b-adrenergic antagonist). mRNA expression of alpha 1-adrenergic subtypes was determined for each group. RESULTS The difference between contractile responses related to electrical field stimulation with incubation with PPADS, atropine, 5 MU, BMY-7378, and CED, respectively, was not significant in the control and diabetic groups (P > .05). The electrical field stimulation responses of strips at 0.5-2 Hz without incubation were significantly different between the control and diabetic groups (P < .05). The contractile responses of strips with PPADS + atropine + 5 MU and BMY-7378 incubations in the diabetic group were significantly lower than in the control group in all doses (P < .05), The mRNA expression of alpha-1a-adrenergic in the diabetic group was significantly lower than in the control group (P < .05). No change was found in the expression of mRNA of alpha-1b-adrenergic. CONCLUSION These results support the probability of changes in presynaptic and autonomic receptor sensitivity. We believe that alpha-1a-adrenergic and alpha-1d-adrenergic subtypes should be kept in mind in the treatment of diabetic cystopathy. UROLOGY 80: 951.e9-951.e16, 2012. (C) 2012 Elsevier Inc.