Streptozocin-induced Diabetes Affects Rat Urinary Bladder Response to Autonomic Agents

Kolta, Malak G.; Wallace, Lane J.; Gerald, Michael C.

doi:10.2337/diab.34.9.917

Cited by 44 publications

(20 citation statements)

References 4 publications

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“…1). The modest, but reproducible, increase in maximum contractile response without changes in sensitivity (EC 50 ) to norepinephrine and phenylephrine is consistent with the findings of Kolta et al (10), in which a significant increase in phenylephrine responsiveness in this region from rats diabetic for 6 wk was reported. However, it appears that the changes observed in the bladder base of diabetic rats are not due to the metabolic alterations in nerve or muscle function but instead occur as a result of diuresis.…”

Section: Discussionsupporting

confidence: 88%

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Effects of Diabetes and Diuresis on Contraction and Relaxation Mechanisms in Rat Urinary Bladder

Kudlacz

Gerald²,

Wallace³

1989

Diabetes

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Experiments were designed to gain information on the mechanisms leading to diabetic urinary bladder dysfunction. Bladders from control rats, animals subjected to 4-5 wk streptozocin-induced diabetes, and rats subjected to equivalent diuresis produced by 5% sucrose feeding were studied with an in vitro whole-bladder preparation and neurochemical measurements. The diuretic group was used to distinguish alterations produced by metabolic effects on nerve and muscle from those induced by prolonged periods of excessive diuresis. Diuresis alone explains many of the diabetes-induced effects, including decreased norepinephrine levels, postsynaptic supersensitivity for sympathetic regulation of bladder storage, decreased responsiveness to parasympathetic regulation of emptying, and enhanced prostaglandin F2 alpha-induced contraction. Other diabetes-induced effects were not observed in the diuretic controls and are presumed to result from metabolic alterations associated with diabetes. These effects were decreases in norepinephrine uptake and in choline acetyltransferase activity, both markers of nerve terminal function. Thus, diuretic and metabolic factors appear to contribute to the early signs of parasympathetic and sympathetic neuropathy. In contrast, we found no evidence for loss of sensory nerve function in the diabetic bladder, at least at the organ level, because no diabetes- or diuresis-induced changes were observed in responsiveness to substance P or capsaicin.

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Section: Discussionsupporting

confidence: 88%

“…In contrast with data on nerves, data from experiments on smooth muscle have not been consistent. Diabetic bladder body muscle strips are reported to be more (10), less (11), or as responsive (7) to cholinergic agonists. Likewise, various conclusions are reported from measurement responsiveness to pelvic nerve stimulation (7,(11)(12)(13).…”

mentioning

confidence: 98%

Effects of Diabetes and Diuresis on Contraction and Relaxation Mechanisms in Rat Urinary Bladder

Kudlacz

Gerald²,

Wallace³

1989

Diabetes

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“…Taken together, these data support the development of a relatively hypocontractile state in diabetes, particularly as the disease future science group future science group progresses. Still, it is clear that not all animal models have shown similar findings and detrusor overactivity, which has also been described, could be explained by the muscarinic supersensitivity described above [4,5]. The cause of detrusor functional alterations is unclear, but altered electrical coupling between adjacent smooth muscle cells, smooth muscle ultrastructural changes, neuronal remodeling and diminished neurotrophic factor expression have all been proposed as a mechanisms underlying diabetes-induced detrusor dysfunction [6,7].…”

Section: Physiology Of Bladder Dysfunction In Diabetesmentioning

confidence: 83%

Lower Urinary Tract Dysfunction in the Diabetic Elderly

Lemack¹

2007

Aging Health

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Elderly patients with diabetes appear to be particularly susceptible to urological complications. Diabetes impacts the urological quality of life as bothersome urinary symptoms (including incontinence) are clearly associated with the development and progression of diabetes. When recognized early, many symptoms can be treated through a combination of behavioral and pharmacological management. Without attention to the early signs of urinary symptoms in elderly patients, significant urological dysfunction may occur, leading to morbidity and often-preventable symptomatic deterioration.It has been estimated that diabetes affects over 246 million people worldwide, with the prevalence clearly on the rise over the last several decades [101]. Indeed, the prevalence of this condition may double by the year 2030. Among those hardest hit by this condition are the elderly, in whom systemic manifestations, such as retinopathy, peripheral neuropathy and nephropathy can result in serious and costly health consequences. The WHO has estimated that in 2007, US$232 billion will be spent worldwide to evaluate and treat diabetes, and that 6% of all deaths are attributable to complications associated with diabetes.Bladder dysfunction in the setting of diabetes, often referred to as diabetic cystopathy, is perhaps more poorly defined and certainly less well recognized that some of the other manifestations of diabetes [1]. Still, it has been estimated that up to 50% of diabetic patients will experience complications related to neurogenic bladder dysfunction resulting from diabetes [2]. Clinical manifestations may start out innocuous, an occasional urinary tract infection or mild urinary frequency, but ultimately can become quite severe. Debilitating urinary incontinence, acute and chronic pyelonephritis, and even renal failure related to a progressive impairment in detrusor function have all been described in diabetic patients. As with other sequelae of diabetes, the early clinical signs of neurogenic bladder dysfunction may be difficult to recognize, often leading to late diagnosis and a missed opportunity for early prevention of serious complications.In the current review, we will first focus on the physiological basis for lower urinary tract dysfunction in diabetic patients and describe the clinical manifestations of that dysfunction. The tools utilized to evaluate bladder dysfunction are discussed, with the typical findings of diabetic patients highlighted. Last, we offer recommendations for recognizing and treating bladder dysfunction related to diabetes, with the goal of minimizing urological complications.

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“…Rats with chemically induced diabetes also develop bladder enlargement, failure to empty, and increased voiding frequency [21,22]. These symptoms are a consequence of autonomic neuropathy in neural pathways to the bladder, diuresis-induced myopathy, and alterations in adrenergic or cholinergic receptors in smooth bladder muscle [21][22][23].…”

Section: Pathophysiologymentioning

confidence: 98%