Progressive Vascular Damage May Lead to Bladder Underactivity in Rats

Nomiya, Masanori; Yamaguchi, Osamu; Akaihata, Hidenori; Hata, Junya; Sawada, Norifumi; Kojima, Yoshiyuki; Andersson, Karl‐Erik

doi:10.1016/j.juro.2013.10.097

Cited by 60 publications

(69 citation statements)

References 27 publications

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“…Atherosclerosis enhanced the expression of inflammatory cytokines, increased oxidative stress, and functionally led to increased voiding frequency. These investigators also compared the effects of a high-cholesterol diet to rats for 8 weeks combined with either iliac artery balloon injury, treatment with the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME) or both, to rats receiving none of the three interventions (Nomiya et al 2014). While L-NAME alone did not change wall thickness of the iliac artery, this was increased by balloon injury and further increased by L-NAME plus balloon injury.…”

Section: Effects Of Chronic Hypoperfusion Of the Bladdermentioning

confidence: 99%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Bladder dysfunction is common in the general population (Stewart et al. 2010) and even more so among patients seeing a physician for any reason (Goepel et al. 2002). It often manifests as lower urinary tract symptoms (LUTS), a term originally coined to describe voiding and storage symptoms in men with benign prostatic hyperplasia (BPH) but now more universally used to describe any type of voiding and storage symptoms in both sexes. Studies into possible causes of urinary bladder dysfunction have long focused on detrusor smooth muscle cells (Turner and Brading 1999). More recently, it became clear that several other types of cells and organs contribute to regulating detrusor smooth muscle function. These include the urothelium (Andersson and McCloskey 2014; Michel 2015), afferent nerves (Michel and Igawa 2015; Yoshimura et al. 2014b), and the central and autonomic nervous systems (Fowler and Griffiths 2010; Yoshimura et al. 2014a). Alterations in any of these may at least partly be responsible for detrusor dysfunction and, accordingly, be potential targets for the treatment of bladder dysfunction. As highlighted by an article in this issue of Naunyn-Schmiedeberg's Archives of Pharmacology (Bayrak et al. 2015), there is an additional suspect, the bladder vasculature. This article will discuss the currently available experimental and clinical evidence for a role of the vasculature in causing bladder dysfunction, and how existing and emerging treatments may modulate bladder function by acting on blood vessels. Due to a similarity in concept, data on prostate perfusion will also be discussed to some extent.

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Section: Effects Of Chronic Hypoperfusion Of the Bladdermentioning

confidence: 99%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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“…The role of the vasculature in bladder function has received relatively little research attention, despite the fact that prolonged decreases in bladder blood flow are linked to both overactive and underactive bladder (28,45). In the present study, we investigated the properties of bladder feed arterioles to determine how these vessels might regulate bladder blood flow during normal bladder function.…”

Section: Discussionmentioning

confidence: 96%

Inhibition of vascular smooth muscle inward-rectifier K⁺channels restores myogenic tone in mouse urinary bladder arterioles

Tykocki

Bonev

Longden

et al. 2017

American Journal of Physiology-Renal Physiology

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“…Therefore, an increase in BBF induced by silodosin may improve bladder contractility by preventing fibrosis of smooth muscle. Since it has been suggested by animal studies that bladder ischemia may cause bladder dysfunction, including bladder overactivity and bladder underactivity [4,33] , silodosin may not only improve bladder overactivity but also prevent the progression to bladder underactivity. Another possible reason for the impaired bladder contractility is a decrease in muscarinic M3 receptor level.…”

Section: Discussionmentioning

confidence: 99%

Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, May Ameliorate Ischemia-Induced Bladder Denervation and Detrusor Dysfunction by Improving Bladder Blood Flow

Goi

Tomiyama²,

Maruyama³

et al. 2016

Pharmacology

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Background/Aims: This study was performed to investigate the detailed mechanism underlying the effects of the selective α_1A-adrenoceptor antagonist, silodosin, on bladder function in a rat model of atherosclerosis-induced chronic bladder ischemia (CBI). Methods: The CBI model was prepared by balloon endothelial injury of the bilateral iliac arteries in male rats. Using an osmotic pump, the CBI rats received either silodosin or vehicle alone subcutaneously for 8 weeks. Rats received a 2% cholesterol diet throughout the experiment. Bladder blood flow (BBF) was measured. Immunohistochemical staining was performed to determine the nerve distribution and nerve growth factor expression in the bladder. Bladders were used for muscle strip contraction analysis. The expression levels of muscarinic M2 and M3 receptors were measured. Results: Silodosin abrogated the decrease in BBF in CBI rats. Silodosin prevented the decrease in nerve distribution and increase in nerve growth factor expression in the CBI model. Bladder contractile response was reduced in the CBI group. Silodosin ameliorated the effect on the bladder contractile response. The level of muscarinic M3 receptor mRNA present in the bladder of CBI rats was increased by silodosin. Conclusion: The results of this study suggest that silodosin ameliorates the denervation of the bladder and effects on detrusor contractile function under ischemic conditions by restoring BBF.

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Progressive Vascular Damage May Lead to Bladder Underactivity in Rats

Abstract: Pelvic arterial occlusive disease plus vascular endothelial dysfunction may cause progressive vascular damage resulting in bladder dysfunction that develops from bladder hyperactivity to bladder underactivity.

Cited by 60 publications

References 27 publications

Are blood vessels a target to treat lower urinary tract dysfunction?

Are blood vessels a target to treat lower urinary tract dysfunction?

Inhibition of vascular smooth muscle inward-rectifier K⁺channels restores myogenic tone in mouse urinary bladder arterioles

Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, May Ameliorate Ischemia-Induced Bladder Denervation and Detrusor Dysfunction by Improving Bladder Blood Flow

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Progressive Vascular Damage May Lead to Bladder Underactivity in Rats

Abstract: Pelvic arterial occlusive disease plus vascular endothelial dysfunction may cause progressive vascular damage resulting in bladder dysfunction that develops from bladder hyperactivity to bladder underactivity.

Cited by 60 publications

References 27 publications

Are blood vessels a target to treat lower urinary tract dysfunction?

Are blood vessels a target to treat lower urinary tract dysfunction?

Inhibition of vascular smooth muscle inward-rectifier K+channels restores myogenic tone in mouse urinary bladder arterioles

Silodosin, an α<sub>1A</sub>-Adrenoceptor Antagonist, May Ameliorate Ischemia-Induced Bladder Denervation and Detrusor Dysfunction by Improving Bladder Blood Flow

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Inhibition of vascular smooth muscle inward-rectifier K⁺channels restores myogenic tone in mouse urinary bladder arterioles