title: Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes.
abstract: Diabetic bladder dysfunction (DBD) is among the most common and bothersome complications of diabetes mellitus. Autonomic neuropathy has been counted as the cause of DBD. In the present study, we compared the alterations in the neurogenically mediated contractile responses of urinary bladder in rats with streptozocin-induced diabetes, 5% sucrose-induced diuresis, and age-matched controls. Male Sprague-Dawley rats were divided into three groups: 9-wk diabetic rats, diuretic rats, and age-matched controls. Micturition and morphometric characteristics were evaluated using metabolic cage and gross examination of the bladder. Bladder detrusor muscle strips were exposed to either periodic electrical field stimulation (EFS) or to EFS in the presence of atropine, alpha,beta-methylene adrenasine 5'-triphosphate, or tetrodotoxin. The proportions of cholinergic, purinergic, and residual nonadrenergic-noncholinergic (NANC) components of contractile response were compared among the three groups of animals. Diabetes caused a significant reduction of body weight compared with diuresis and controls, although the bladders of diabetic and diuretic rats weighed more than the controls. Both diabetes and diuresis caused significant increase in fluid intake, urine output, and bladder size. Diabetes and diuresis caused similarly increased response to EFS and reduced response to cholinergic component compared with controls. However, the purinergic response was significantly smaller in diuretic bladder strips compared with controls but not in diabetic rats. A residual NANC of unknown origin increased significantly but differently in diabetics and diuretics compared with controls. In conclusion, neurogenically mediated bladder contraction is altered in the diabetic rat. Diabetic-related changes do not parallel diuretic-induced changes, indicating that the pathogenesis of DBD needs further exploration.
authors.affiliation: Glickman Urological Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
authors.forename: Guiming
authors.initials: G
authors.lastname: Liu
authors.forename: Firouz
authors.initials: F
authors.lastname: Daneshgari
mesh_terms: D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D002799:Cholinergic Fibers / Q000502:physiology; D048909:Diabetes Complications / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D004231:Diuresis / Q000502:physiology; D004558:Electric Stimulation; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D009130:Muscle, Smooth / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D001743:Urinary Bladder / Q000294:innervation / Q000503:physiopathology*; D014555:Urination Disorders / Q000503:physiopathology*
chemical_list: D000109:Acetylcholine; D009638:Norepinephrine