Effect of tamsulosin on spontaneous bladder contraction in conscious rats with bladder outlet obstruction: Comparison with effect on intraurethral pressure

Ohtake, Akiyoshi; Ukai, Masashi; Saitoh, Chikashi; Sonoda, Rie; Noguchi, Yukiko; Okutsu, Hiroko; Yuyama, Hironori; Sato, Shuichi; Sasamata, Masao; Miyata, Keiji

doi:10.1016/j.ejphar.2006.06.054

Cited by 31 publications

(26 citation statements)

References 36 publications

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“…Female continence structures are ␣ 1 -adrenergic in origin and a high concentration of ␣ 1 -adrenergic receptors are found at the bladder neck, the urethra and in periurethral tissue while ␤ -adrenergic receptors are markedly more prevalent on the remaining detrusor surface. Consequently, stimulation of the sympathetic nervous system will trigger bladder relaxation which guarantees filling and, at the same time, contraction of continence structures [16] . A study in female and male rabbits compared the sex-specific density and affinity of ␣ 1 -adrenergic receptors and indicated no difference [17] .…”

Section: Discussionmentioning

confidence: 99%

Open-Label, Longitudinal Study of Tamsulosin for Functional Bladder Outlet Obstruction in Women

et al. 2009

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Objectives: To investigate the clinical effect of tamsulosin for the treatment of functional bladder outlet obstruction (BOO) in adult women. Methods: In a prospective, longitudinal open-label study, 63 women affected by functional BOO were treated with tamsulosin. Inclusion criteria were: age >18 years, reporting voiding symptoms (intermittent stream, hesitancy, straining and/or a feeling of incomplete emptying), uroflowmetry maximum flow rate (Q_max) under 12 ml and/or presence of postvoid residual greater than 50% of the voiding volume. Exclusion criteria were: patients suffering from any other anatomical or functional disorder such as urethral stenosis, pelvic organ prolapse, neurological disturbances, or systemic diseases that could impact upon bladder voiding. Tamsulosin was administered in a single daily dose of 0.4 mg for at least 30 days. Primary outcomes were clinical efficacy and Q_max improvement; secondary outcomes were tolerability and safety. Voiding and storage symptoms and uroflowmetry results were assessed before and at the end of the α-blocker therapy. Results: Tamsulosin therapy was well tolerated. After therapy voiding symptoms improved in 71.4% of patients (45/63; p < 0.0001), and if associated with storage symptoms in 66.67% (26/39; p < 0.00001). Recurrent infections were reduced by 50% in 81% (21/26) of patients. Uroflowmetry parameters improved in 36/63 patients (57.1%). Postvoiding residue improved in 62.5% (10/16) and disappeared in 25% (4/16) with no significant changes in voided volume. An improvement was observed in 66% (16/24) of patients with isolated voiding symptoms, in 51.2% (20/39) with associated storage symptoms and in 65% (17/26) of women with associated recurrent urinary infections. Conclusions: These results suggest that α-blocker may be an effective treatment option in women with voiding dysfunction due to functional BOO.

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Section: Discussionmentioning

confidence: 99%

Open-Label, Longitudinal Study of Tamsulosin for Functional Bladder Outlet Obstruction in Women

et al. 2009

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“…Although this concept is still accepted and may be true, it is now clear that mechanisms besides prostate smooth muscle relaxation contribute to the beneficial effects of α 1 ‐blockers during treatment of LUTS in BPH patients . In animal models, where BOO is simulated by partial urethral obstruction and a prostate‐dependent contribution can be excluded, α 1 ‐blockers effectively improved storage symptoms . Moreover, improvement of LUTS by α 1 ‐blockers was observed in men without BPO, and occurs without relieving the obstruction .…”

Section: Introductionmentioning

confidence: 99%

Prostatic α1‐adrenoceptors: New concepts of function, regulation, and intracellular signaling

Hennenberg

Stief

Gratzke

2013

Neurourology and Urodynamics

205

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Prostatic α1 -adrenoceptors are known to be involved in the pathophysiology of lower urinary tract symptoms (LUTS) in patients with benign prostate obstruction (BPO). It is widely accepted that enhanced α1 -adrenergic smooth muscle contraction can contribute to bladder outlet obstruction; α1 -adrenoceptor antagonists still represent a gold standard in the treatment of LUTS. Accordingly, expression and function of α1 -adrenoceptors in the prostate have attracted large attention over the last three decades. However, recent preclinical studies have challenged our understanding of prostatic α1 -adrenoceptors. In the current review article, we summarize "modern" concepts of prostatic α1 -adrenoceptors which include novel intracellular mediators of contraction as well as non-contractile signaling and post-translational receptor regulation. Configuration of α1 -adrenoceptors with binding partners may determine its function, leading to a dynamic receptor with high functional plasticity. Cooperative regulation of different intracellular effectors (MAPK, Akt, transcription factors) by α1 -adrenoceptors, hormones or growth factors has been suggested. The prostatic α1 -adrenoceptor is no longer being regarded as an isolated, static receptor exclusively mediating prostatic smooth muscle contraction by G proteins, but a dynamic receptor interacting with other receptors within a complex network of mediators.

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“…Therefore, it is a possible explanation to positive effect noted in the animals treated with tamsulosin on the filling phase. In one of these studies the effect of tamsulosin on the bladder function was investigated in conscious rats with bladder outlet obstruction induced by partial urethral ligation, and was concluded that premicturition contractions observed in obstructed rats were reduced with alpha-(1)--adrenoceptor antagonists (19). However, further studies are necessary to determine the mechanisms behind the effects of tamsulosin at bladder.…”

Section: Discussionmentioning

confidence: 99%

Effects of chronic administration of tamsulosin and tadalafil, alone or in combination, in rats with bladder outlet obstruction induced by chronic nitric oxide deficiency

et al. 2014

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ARTICLE INFO ______________________________________________________________ ______________________Purpose: The aim of this study was to define if tadalafil causes detrusor muscle impairment and to observe the effect of combination of tadalafil with tamsulosin on the lower urinary tract of rats with bladder outlet obstruction (BOO) induced by chronic nitric oxide deficiency. Materials and Methods: Thirty-one male rats were randomized to following groups: 1 -control; 2 -L-Nitroarginine methyl ester (L-NAME); 3 -Tamsulosin + L-NAME, 4 Tadalafil+L-NAME; and 5 -Tamsulosin + Tadalafil + L-NAME. At the end of the treatment period (30 days), all animals were submitted to urodynamic study. Results:The administration of L-NAME increased the number of non-voiding contractions (NVC) (1.04 ± 0.22), volume threshold (VT) (1.86 ± 0.35), and micturition cycle (MC) (1.34 ± 0.11) compared with control (0.52 ± 0.06, 0.62 ± 0.06, and 0.67 ± 0.30), respectively. The administration of tamsulosin reduced the number of NVC (0.57 ± 0.42) and VT (0.76 ± 0.24 ) compared with L-NAME group. Co-treatment with tadalafil decreased the number of VT (0.85 ± 0.53) and MC (0.76 ± 0.22) compared with L-NA-ME group. The combination of tamsulosin with tadalafil improved the number of NVC (0.56 ± 0.18), VT (0.97 ± 0.52) and MC (0.68 ± 0.30) compared with L-NAME group. Conclusion: In rats with BOO induced by chronic nitric oxide deficiency, tadalafil did not cause impairment in detrusor muscle and seems to have an addictive effect to tamsulosin because the combination decreased non voiding contractions as well the number of micturition cycles.

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Effect of tamsulosin on spontaneous bladder contraction in conscious rats with bladder outlet obstruction: Comparison with effect on intraurethral pressure

Cited by 31 publications

References 36 publications

Open-Label, Longitudinal Study of Tamsulosin for Functional Bladder Outlet Obstruction in Women

Open-Label, Longitudinal Study of Tamsulosin for Functional Bladder Outlet Obstruction in Women

Prostatic α1‐adrenoceptors: New concepts of function, regulation, and intracellular signaling

Effects of chronic administration of tamsulosin and tadalafil, alone or in combination, in rats with bladder outlet obstruction induced by chronic nitric oxide deficiency

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