Effect of Tamsulosin on Bladder Microcirculation in Rat Model of Bladder Outlet Obstruction Using Pencil Lens Charge-coupled Device Microscopy System

Mine, Shotarou; Yamamoto, Takatsugu; Mizuno, Hideki; Endo, Kanako; Matsukawa, Yoshihisa; Funahashi, Yasuhito; Kato, Masashi; Hattori, Ryohei; Gotoh, Momokazu

doi:10.1016/j.urology.2012.09.008

Cited by 13 publications

(12 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, in a rat BOO model, treatment with tamsulosin restored perfusion and increased voided volume . Such findings were confirmed by other investigators using a different experimental approach (Mine et al 2013). Another α 1 -adrenoceptor antagonist, silodosin, restored bladder perfusion in spontaneously hypertensive rats, which exhibit an OABlike phenotype (Inoue et al 2012).…”

Section: Effects Of Therapeutics On Bladder Perfusionsupporting

confidence: 66%

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

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

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.

show abstract

Section: Effects Of Therapeutics On Bladder Perfusionsupporting

confidence: 66%

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

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

show abstract

“…Thus, an elevated sympathetic nerve input to suburothelial microvasculature, that may be associated with hypertension or cardiac failure, would increase the resistance to blood circulation resulting in bladder overactivity. Therefore, it is reasonable to assume that the improvement of bladder storage function with α-adrenoceptor antagonists may be partly attributed to dilatation of the suburothelial microvasculature [22]. Such vasodilatating effects of α-adrenoceptor would be beneficial for not only improving blood supply to the tissue but also correcting tissue acidification which appears to play a critical role in the induction of urinary urgency.…”

Section: Discussionmentioning

confidence: 99%

“…Of studies that examine bladder venules, it is suggested that diminished venular drainage can result in tissue metabolite accumulation and contribute to 'urinary urgency' upon acidification-induced stimulation of TRP channels at sensory nerve endings [8,20]. Thus it is reasonable to assume that improvement of bladder storage symptoms with α-adrenoceptor antagonists [22] or PDE5 inhibitors [25] may be attributed to their vasodilator action on the suburothelial microvasculature. β 3 -Adrenoceptor agonists may also exert an influence by improving the microcirculation within the bladder wall [1].…”

Section: Introductionmentioning

confidence: 99%

Neurohumoral regulation of spontaneous constrictions in suburothelial venules of the rat urinary bladder

Shimizu

Mochizuki

Mitsui

et al. 2014

Vascular Pharmacology

View full text Add to dashboard Cite

“…α 1 -Adrenoceptor antagonists induce increases in bladder blood flow (BBF) and bladder capacity in LUTS patients [9] . Treatment with α 1A -adrenoceptor-selective drugs but not α 1D -adrenoceptor-selective drugs improves BBF in animal models, such as bladder outlet obstruction [10] , spontaneously hypertensive rats [11,12] , and CBI [13] . The distributions of the various α 1 -adrenoceptor subtypes in each tissue have been reported [14] .…”

Section: Introductionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Effect of Tamsulosin on Bladder Microcirculation in Rat Model of Bladder Outlet Obstruction Using Pencil Lens Charge-coupled Device Microscopy System

Cited by 13 publications

References 18 publications

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

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

Neurohumoral regulation of spontaneous constrictions in suburothelial venules of the rat urinary bladder

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

Contact Info

Product

Resources

About