Pathophysiological mechanisms in detrusor underactivity: Novel experimental findings

Abstract

Underactive bladder (UAB) is a multifactorial symptom complex often related to detrusor underactivity (DU). Although recognized as a common cause of lower urinary tract symptoms and with significant effects on quality of life, UAB/DU is largely underresearched. Herein, we review upto-date knowledge on the pathophysiological mechanisms of UAB/DU, with an emphasis on the relationship between UAB and bladder outlet obstruction (BOO). Original articles and reviews concerning UAB/DU were identified through a search of the PubMed/Medline and Scopus databases. DU can result from several pathological mechanisms, which can be categorized as idiopathic, neurogenic, myogenic, or functional. The main etiological factors of UAB/DU are aging, diabetes mellitus, neurogenic disorders, and BOO. Although conventional models focus primarily on efferent nerve and myogenic mechanisms, contemporary views highlight the importance of the afferent pathway. Specifically, recent findings in BOO showed that afferent dysfunction, such as altered expression of muscarinic and purinergic P2X 3 receptors or diminished urothelial ATP may play a role in the initial and reversible stages of DU, with potential diagnostic and therapeutic implications. K E Y W O R D S bladder outlet obstruction, detrusor underactivity, lower urinary tract symptoms, pathophysiology

Bladder overactivity and post-void residual: Which relates more to systemic atherosclerotic markers?

“…One possibility is due to a small sample size. The other possibility is that, while gender did not contribute to either detrusor overactivity or CAVI significantly in the previous studies, female gender might have lessened CAVI as suggested by a recent paper (Emi et al, 2008;Hsiao et al, 2014;Osman et al, 2018;Sakakibara et al, 2014;Smith et al, 2016;Suzuki et al, 2013;Uzun et al, 2013;Vale et al, 2019;Yeniel et al, 2018;Zacche et al, 2017). In addition, the mechanism of underactive detrusor includes 1) intrinsic detrusor muscle change by ageing, 2) secondary phenomenon by prolonged DO particularly in outlet obstruction, and 3) neural damage in the peripheral nerves (diabetes, lumbar spondylosis, etc.)…”

“…In addition, the mechanism of underactive detrusor includes 1) intrinsic detrusor muscle change by ageing, 2) secondary phenomenon by prolonged DO particularly in outlet obstruction, and 3) neural damage in the peripheral nerves (diabetes, lumbar spondylosis, etc.) and/or spinal cord (DHIC as described above) (Osman et al, 2018;Vale et al, 2019). Among these, we could not answer the mechanism of prolonged DO.…”

EP2 and EP3 receptors as therapeutic targets for underactive bladder/detrusor underactivity due to diabetic cystopathy in a type 1 diabetic rat model

“…In contrast to our previous study using the LCS rat model, in which ONO-8055 significantly decreased MCC, 24 24,26,27 This means that UAB/DU is much more severe in the LCS model than the T1D model. In addition, the T1D model is supposed to be a myogenic rather than a neurogenic UAB/DU model, 3 while the LCS model is supposed to be a neurogenic rather This study has several limitations. First, we did not measure UPP, although a previous study showed a decrease in UPP in the LCS model after administration of TAM and ONO-8055.…”

“…1 UAB is a major problem that is not well known in the public and health care sectors but is an enormous economic problem that will become more prevalent with the increasing age of populations. The etiology of UAB/DU includes aging as well as neurological diseases, and, above all, diabetic cystopathy (DC) is a major etiology of UAB/DU, [1][2][3] which affects over 50% of diabetic patients, 4 ranging from 25% to 90%. 5 The global prevalence of diabetes is estimated at 9.3% (463 million people) worldwide, and it increases with age, reaching 19.9% (111.2 million people) at 65 to 79 years old.…”

Detrusor Underactivity and Underactive Bladder in Women: What Is New?

“…The influence of pelvic arterial ischaemia on bladder function is generating increasing interest [11]. Experiments in rodents have shown that inducing ischaemia in the pelvic vasculature leads to ischaemia in the bladder wall and impaired oxygenation.…”