Metabolic Syndrome and LUTS/BPH

Gacci, Mauro; Sebastianelli, Arcangelo; Salvi, Matteo

doi:10.1016/b978-0-12-811397-4.00005-6

Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia 2018

DOI: 10.1016/b978-0-12-811397-4.00005-6

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Metabolic Syndrome and LUTS/BPH

Mauro Gacci

Arcangelo Sebastianelli

Matteo Salvi

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2023

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Cited by 1 publication

(2 citation statements)

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“…Interactions between the UBSM and the ECM control both basal smooth muscle tone as well as non-voiding transient pressure events that drive the majority of sensory outflow to the central nervous system 15 . Because the stiffness and elasticity of the bladder wall tissue is imparted by properties of both UBSM and ECM, altered muscle tone and collagen content are present in many bladder pathologies 16 .Lower urinary tract symptoms (LUTS), including frequency, urgency and urge incontinence, are often associated with both an alteration in clinical compliance as well as bladder inflammation [17][18][19] . The pathogenesis of inflammatory bladder remodeling is also associated with the degranulation of mast cells present within the bladder wall 20,21 .…”

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confidence: 99%

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Compound 48/80 increases murine bladder wall compliance independent of mast cells

Saxena

Broemer

Herrera

et al. 2023

Sci Rep

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A balance between stiffness and compliance is essential to normal bladder function, and changes in the mechanical properties of the bladder wall occur in many bladder pathologies. These changes are often associated with the release of basic secretagogues that in turn drive the release of inflammatory mediators from mast cells. Mast cell degranulation by basic secretagogues is thought to occur by activating an orphan receptor, Mas-related G protein-coupled receptor B2 (Mrgprb2). We explored the effects of the putative mast cell degranulator and Mrgprb2 agonist Compound 48/80 on urinary bladder wall mechanical compliance, smooth muscle contractility, and urodynamics, and if these effects were mast cell dependent. In wild-type mice, Mrgprb2 receptor mRNA was expressed in both the urothelium and smooth muscle layers. Intravesical instillation of Compound 48/80 decreased intermicturition interval and void volume, indicative of bladder overactivity. Compound 48/80 also increased bladder compliance while simultaneously increasing the amplitude and leading slope of transient pressure events during ex vivo filling and these effects were inhibited by the Mrgprb2 antagonist QWF. Surprisingly, all effects of Compound 48/80 persisted in mast cell-deficient mice, suggesting these effects were independent of mast cells. These findings suggest that Compound 48/80 degrades extracellular matrix and increases urinary bladder smooth muscle excitability through activation of Mrgprb2 receptors located outside of mast cells. Thus, the pharmacology and physiology of Mrgprb2 in the urinary bladder is of potential interest and importance in terms of treating lower urinary tract dysfunction.

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mentioning

confidence: 99%

“…Lower urinary tract symptoms (LUTS), including frequency, urgency and urge incontinence, are often associated with both an alteration in clinical compliance as well as bladder inflammation [17][18][19] . The pathogenesis of inflammatory bladder remodeling is also associated with the degranulation of mast cells present within the bladder wall 20,21 .…”

mentioning

confidence: 99%

Compound 48/80 increases murine bladder wall compliance independent of mast cells

Saxena

Broemer

Herrera

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

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Metabolic Syndrome and LUTS/BPH

Cited by 1 publication

References 92 publications

Compound 48/80 increases murine bladder wall compliance independent of mast cells

Compound 48/80 increases murine bladder wall compliance independent of mast cells

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