Abstract
Urinary incontinence resulting from abnormal bladder function is an extremely common problem affecting millions of men and women around the globe. Many diseases, such as stroke, diabetes mellitus, and benign prostatic hyperplasia (BPH), as well as the ravages of advancing age, contribute to altered bladder function. While urinary incontinence is clearly a multifactorial disease, one prevalent manifestation, known as urge incontinence, is related to uncontrolled and involuntary bladder contractions (i.e., bladder overactivity). This overactivity is the result of increased detrusor smooth muscle contractions. The precise physiological mechanisms contributing to the overactive bladder are not clearly understood. However, two different hypotheses, myogenic4 and neurogenic,21 have been advanced. The extant clinical and laboratory data support both hypotheses, but this report will focus exclusively on myogenic considerations. However, it should be emphasized that regardless of the precise etiologic cause of bladder hyperactivity, the physiological impact is the same; detrusor myocytes contract spontaneously, causing urinary incontinence.
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Christ, G.J. et al. (2003). Intercellular Communication and Bladder Function. In: Atala, A., Slade, D. (eds) Bladder Disease, Part A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-8889-8_17
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DOI: https://doi.org/10.1007/978-1-4419-8889-8_17
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