ABSTRACT
Computerized data acquisition was used to achieve a comprehensive assessment of micturition and cystometry in rats made diabetic with streptozotocin. Diabetic rats had a greater mean voided volume and a significantly shorter interval between voiding during the light cycle. During volume expulsion, the rate of intraluminal pressure development was greater, but the mean duration of volume expulsion was less in the diabetic bladder. The increased rate of intraluminal pressure development in the diabetic bladder at the time of volume expulsion correlated with the greater tension development in bladder body strips in response to acetylcholine stimulation. The inability of the diabetic bladder body to maintain peak intraluminal pressure may contribute to the development of residual urine, increased bladder volume and increased voiding frequency in the diabetic rat.
Subject(s)
Diabetes Mellitus, Experimental/physiopathology , Muscle Contraction/physiology , Urinary Bladder/physiopathology , Urination/physiology , Acetylcholine/pharmacology , Animals , Circadian Rhythm , Cystoscopy , Male , Muscle, Smooth/physiology , Rats , Rats, Sprague-Dawley , Signal Processing, Computer-AssistedABSTRACT
The in vitro effects of a calcium channel agonist (BAY K8644) and antagonist (nifedipine) on the cholinergic responses of the streptozotocin-induced diabetic rat bladder were investigated. the bladder body and bladder base were studied separately. There were significant differences in contractile responses to acetylcholine stimulation in the diabetic bladder body compared to the control body. Similarly, the diabetic bladder base demonstrated significantly increased contractile responses compared to the control base. Contractile responses in the diabetic bladder body and base were significantly increased from the control in the absence of extracellular calcium. Differences were found in the effects on maximum responses between diabetic and control tissues treated with nifedipine and BAY K8644. BAY K8644 did not completely reverse the effect of nifedipine on the contractile responses. Rates of contractile response were significantly different between controls and diabetics and between body and base. Alterations in calcium channel activity in diabetic bladder smooth muscle may be responsible at least in part for the nonspecific pharmacologic responses found in smooth muscle strips.
Subject(s)
Calcium Channels/physiology , Diabetes Mellitus, Experimental/physiopathology , Urinary Bladder/physiopathology , 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester/pharmacology , Acetylcholine/pharmacology , Animals , Calcium Channels/drug effects , In Vitro Techniques , Male , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Muscle, Smooth/physiopathology , Nifedipine/pharmacology , Rats , Rats, Inbred Strains , Urinary Bladder/drug effects , Urinary Bladder/innervationABSTRACT
The in vitro effects of a calcium channel antagonist (nifedipine) and agonist (BAY K8644) on the neurogenic responses of the streptozotocin-induced diabetic rat bladder were investigated. The bladder body and bladder base were studied separately. There were no significant differences in neurogenic responses in diabetic bladder body compared to control body, but the diabetic bladder base demonstrated an increased contractile response at each frequency compared to control base. The rate of contractile response was similar in controls and diabetics but was significantly different between body and base. Although declining with time, contractile responses in the diabetic bladder body and base were increased from control in the absence of extracellular calcium. Differences were found in effects upon maximum responses between diabetic and control tissues treated with nifedipine and BAY K8644. BAY K8644 did not completely reverse the effect of nifedipine on the neurogenic responses in the diabetic bladder body. Effects of diabetes on the bladder body and base are associated with changes in calcium channel activity of bladder smooth muscle.
