Characterization of the urinary bladder dysfunction in renovascular hypertensive rats

Ramos-Filho, Antonio Celso Saragossa; Mónica, Fabíola Z.; Franco‐Penteado, Carla F.; Rojas-Moscoso, Julio Alejandro; Báu, Fernando R.; Schenka, André Almeida; Nucci, Gilberto De; Antunes, Edson

doi:10.1002/nau.21074

Cited by 14 publications

(9 citation statements)

References 54 publications

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“…The β3 agonist, BRL 373444 increased transient, spontaneous, outward BK current, causing membrane hyperpolarization and this response was eliminated in the presence of iberiotoxin and tetraethylammonium. 22 In animal models of detrusor overactivity such as chronic deprivation of nitric oxide by long-term treatment with L-NAME, 24 hypoxia through the iliac artery injury, 10 and renovascular hypertension, 25 the relaxation induced by β-AR agonists was reduced leading the authors to conclude that the detrusor overactivity seen in these models could be in part due to impairment of the beta-adrenoceptor pathway. In addition to the relaxation in human bladder, 12 mirabegron also relaxed human and rabbit prostatic smooth muscle, 7 suggesting that this drug may be also effective in treating OAB secondary to BPH.…”

Section: Discussionmentioning

confidence: 99%

Long‐term treatment with the beta‐3 adrenoceptor agonist, mirabegron ameliorates detrusor overactivity and restores cyclic adenosine monophosphate (cAMP) levels in obese mice

Calmasini

Oliveira

Alexandre

et al. 2016

Neurourology and Urodynamics

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Section: Discussionmentioning

confidence: 99%

Long‐term treatment with the beta‐3 adrenoceptor agonist, mirabegron ameliorates detrusor overactivity and restores cyclic adenosine monophosphate (cAMP) levels in obese mice

Calmasini

Oliveira

Alexandre

et al. 2016

Neurourology and Urodynamics

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“…Cumulative concentration response curves to CaCl 2 (1 µM to 100 mM) using one log unit increments in depolarizing conditions were constructed, as previously described [19]. Briefly, the strips were prepared and mounted in 10 mL organ baths containing Ca 2+ -free Krebs' solution with EGTA (1 mM) to sequester Ca 2+ ions.…”

Section: Methodsmentioning

confidence: 99%

Menthol Inhibits Detrusor Contractility Independently of TRPM8 Activation

et al. 2014

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Agonists such as icilin and menthol can activate the cool temperature-sensitive ion channel TRPM8. However, biological responses to menthol may occur independently of TRPM8 activation. In the rodent urinary bladder, menthol facilitates the micturition reflex but inhibits muscarinic contractions of the detrusor smooth muscle. The site(s) of TRPM8 expression in the bladder are controversial. In this study we investigated the regulation of bladder contractility in vitro by menthol. Bladder strips from wild type and TRPM8 knockout male mice (25–30 g) were dissected free and mounted in organ baths. Isometric contractions to carbachol (1 nM–30 µM), CaCl2 (1 µM to 100 mM) and electrical field stimulation (EFS; 8, 16, 32 Hz) were measured. Strips from both groups contracted similarly in response to both carbachol and EFS. Menthol (300 µM) or nifedipine (1 µM) inhibited carbachol and EFS-induced contractions in both wild type and TRPM8 knockout bladder strips. Incubation with the sodium channel blocker tetrodotoxin (1 µM), replacement of extracellular sodium with the impermeant cation N-Methyl-D-Glucamine, incubation with a cocktail of potassium channel inhibitors (100 nM charybdotoxin, 1 µM apamin, 10 µM glibenclamide and 1 µM tetraethylammonium) or removal of the urothelium did not affect the inhibitory actions of menthol. Contraction to CaCl2 was markedly inhibited by either menthol or nifedipine. In cultured bladder smooth muscle cells, menthol or nifedipine abrogated the carbachol or KCl-induced increases in [Ca2+]i. Intravesical administration of menthol increased voiding frequency while decreasing peak voiding pressure. We conclude that menthol inhibits muscarinic bladder contractions through blockade of L-type calcium channels, independently of TRPM8 activation.

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“…On the other hand, long‐standing or excessive hypertrophy can also be harmful and become a cause of morbidity and mortality, for instance in the heart . Hypertrophy of the urinary bladder has often been studied in the context of bladder outlet obstruction but it can also occur in the absence of obstruction, for instance in patients with overactive bladder syndrome or obstruction‐independent animal models thereof …”

Section: Introductionmentioning

confidence: 99%

A systematic review of urinary bladder hypertrophy in experimental diabetes: Part I. Streptozotocin‐induced rat models

İnan

Ellenbroek

Michel

2018

Neurourology and Urodynamics

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Aims:To better understand the genesis and consequences of urinary bladder hypertrophy in animal models of diabetes. This part of a three-article series will analyze urinary bladder hypertrophy in the diabetes mellitus type 1 model of rats injected with streptozotocin (STZ). Methods: A systematic search for the key word combination "diabetes," "bladder"and "hypertrophy" was performed in PubMed; additional references were identified from reference lists of those publications. All papers were systematically extracted for relevant information. Results: A total of 39 studies were identified that quantitatively reported on bladder hypertrophy in rats upon injection of STZ; of which several reported on multiple time points yielding a total of 83 group comparisons. Bladder hypertrophy was found consistently, being fully developed as early as 1 week after STZ injection (bladder weight 188 ± 59% of matched control). Hypertrophy was similar across sexes and STZ doses (35-40 vs 50-65 mg/kg) but appeared greater with Wistar rats than other rat strains. The extent of bladder hypertrophy was not correlated to blood glucose concentrations, but normalization of blood glucose concentration by insulin treatment starting early after STZ injection prevented hypertrophy; insulin treatment starting after hypertrophy had established largely reversed it. Conclusions: Bladder size approximately doubles after STZ injection in rats; the extent of hypertrophy is not linked to the severity of hyperglycemia but largely reversible by restoration of euglycemia. K E Y W O R D Sbladder, diabetes, hypertrophy, insulin, rat strain, streptozotocinThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Characterization of the urinary bladder dysfunction in renovascular hypertensive rats

Abstract: Renovascular hypertensive rats exhibit bladder dysfunction that involves tissue remodeling and enhanced muscarinic M(3) -mediated contractions associated with reduced β-adrenoceptor-mediated signal transduction.

Cited by 14 publications

References 54 publications

Long‐term treatment with the beta‐3 adrenoceptor agonist, mirabegron ameliorates detrusor overactivity and restores cyclic adenosine monophosphate (cAMP) levels in obese mice

Long‐term treatment with the beta‐3 adrenoceptor agonist, mirabegron ameliorates detrusor overactivity and restores cyclic adenosine monophosphate (cAMP) levels in obese mice

Menthol Inhibits Detrusor Contractility Independently of TRPM8 Activation

A systematic review of urinary bladder hypertrophy in experimental diabetes: Part I. Streptozotocin‐induced rat models

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