Altered electrical properties of bladder smooth muscle in streptozotocin-induced diabetic rats.
OBJECTIVE
To examine the alterations in the electrical properties of bladder smooth muscle in rats with diabetes mellitus (DM) induced by streptozotocin.


METHODS
The study comprised 34 control rats and 20 with DM induced experimentally by injection with streptozotocin. At 10-15 weeks after the induction of DM, control and treated rats were killed, the bladder removed and the electrical responses of membranes from the detrusor smooth muscle recorded using intracellular microelectrodes.


RESULTS
The resting membrane potential of the smooth muscle remained unaltered by DM but the frequency of spontaneous spike discharges sensitive to nicardipine was decreased. Transmural nerve stimulation elicited a purinergic excitatory junction potential (EJP) in muscles from both types of rat, but the threshold intensity of stimulation required to evoke an EJP was higher in muscle from the diabetic rat. Furthermore, EJPs large enough to trigger a nicardipine-sensitive spike potential could be elicited easily in muscles from the control rat, but not in muscles from diabetic rats. Stimulation of muscarinic receptors with exogenous acetylcholine (ACh) caused greater depolarization in muscle from diabetic rats. Stimulation of purinergic receptors with alpha, beta-methylene ATP caused a similar depolarization in both groups of rats. Application of potassium-free solution or ouabain depolarized the membrane by about 9 mV or 5 mV, respectively, in muscles from both groups of rat. Removal of potassium-free solution produced an ouabain-sensitive transient hyperpolarization which was larger in muscle from control rats, indicating that the potency of the Na-K pump was weakened in rats with DM.


CONCLUSIONS
In the detrusor smooth muscle of rats with DM, there were fewer spontaneous spike discharges, supersensitivity of post-junctional muscarinic receptors, reduced potency of the post-junctional Na-K pump and a decrease in the release of neurotransmitter, possibly due to the impairment of prejunctional activity.
Hashitani
H
H
Department of Physiology, Nagoya City University Medical School, Japan.
Suzuki
H
H
D000109:Acetylcholine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D004594:Electrophysiology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000503:physiopathology*; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D013311:Streptozocin
D010042:Ouabain; D013311:Streptozocin; D000255:Adenosine Triphosphate; D000109:Acetylcholine; C002630:alpha,beta-methyleneadenosine 5'-triphosphate