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Altered electrical properties of bladder smooth muscle in streptozotocin-induced diabetic rats
1Department of Physiology, Nagoya City University Medical School, Japan.
Objective:
To examine the alterations in the electrical properties of bladder smooth muscle in rats with diabetes mellitus (DM) induced by streptozotocin.
Materials And 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.
Conclusion:
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.
Insights
Diabetes mellitus in rats alters bladder smooth muscle electrical properties, reducing spontaneous activity and neurotransmitter release while increasing receptor sensitivity. The Na-K pump
Area of Science:
- Physiology
- Pharmacology
- Urology
Background:
- Diabetes mellitus (DM) is a metabolic disorder with potential complications affecting various organ systems, including the urinary tract.
- Bladder smooth muscle dysfunction can lead to lower urinary tract symptoms, impacting quality of life.
Purpose of the Study:
- To investigate the electrophysiological changes in detrusor smooth muscle of rats with streptozotocin-induced diabetes mellitus.
- To understand the functional consequences of diabetes on bladder smooth muscle contractility and neural control.
Main Methods:
- Experimental induction of diabetes mellitus in rats using streptozotocin.
- Recording of electrical activity in detrusor smooth muscle using intracellular microelectrodes.
- Assessment of responses to nerve stimulation, receptor agonists, and ion-modulating solutions.
Main Results:
- Diabetes reduced spontaneous spike discharge frequency and increased the threshold for excitatory junction potentials (EJPs).
- Diabetic bladders showed supersensitivity to acetylcholine at muscarinic receptors but not purinergic receptors.
- Na-K pump potency was diminished in diabetic rat bladders, indicated by altered responses to potassium-free solution and ouabain.
Conclusions:
- Diabetes mellitus impairs bladder smooth muscle electrical properties, affecting spontaneous activity and neurotransmission.
- Post-junctional muscarinic receptor supersensitivity and reduced Na-K pump function are key alterations in diabetic bladders.
- These changes may contribute to the pathophysiology of bladder dysfunction in diabetes.