Can the beneficial effects of tamsulosin on the overactive bladder be explained by an effect on bladder blood flow?

Damian Nilsson, Donna J Sellers*, Russ Chess-Williams

*Corresponding author for this work

Research output: Contribution to journalMeeting AbstractResearchpeer-review

Abstract

Introduction: Tamsulosin is used in the treatment of bladder outlet obstruction caused by benign prostatic hyperplasia in males. However, it has also been found to be beneficial in the treatment of overactive bladder in both men and women, although the mechanism of this action is unclear. One possible explanation could be an effect on the blood vessels supplying the bladder, where tamsulosin could potentially prevent sympathetic vasoconstriction and enhance bladder blood flow. Indeed, in recent years a number of studies have suggested that lower urinary tract dysfunction, such as overactive bladder, may be caused by reduced blood flow. The objective of this study was to examine the α1-adrenoceptors involved in contraction of the blood vessels supplying to a pig bladder (a good model of the human bladder) and investigate whether tamsulosin and silodosin at clinical doses could influence blood flow to these tissues. Materials & methods: Superior vesical artery branches from pig bladders (6-month old) were obtained from a local abattoir. Sections of artery (~4mm length, ~1mm internal diameter) were isolated and mounted between two horizontal stirrups under physiological conditions (in aerated Krebs-bicarbonate solution at 37˚C). Contractions of the circular muscle of the arteries was recorded in response to phenylephrine, a drug that acts at α1- adrenoceptors. Different subtypes of α1-adrenoceptors exist; however, in this study they were identified using selective antagonists for α1a-adrenoceptors (RS100329) and α1d- drenoceptors (BMY7378). The effects of the α1-adrenoceptor antagonist drugs tamsulosin and silodosin were also investigated. Results: The α1d-adrenoceptor antagonist BMY7378 did not affect contractions of arteries to phenylephrine. However, the α1a-adrenoceptor antagonist S100329 did significantly antagonise contractions to phenylephrine. Both antagonists, tamsulosin and silodosin, significantly antagonised contractions of arteries to phenylephrine, at low doses (Fig. 1). None of the antagonists significantly affected maximal contractions to phenylephrine. Conclusion: The results indicate that the arteries supplying blood to the bladder express the same α1- adrenoceptor subtype as those causing contraction of the human prostate. Both antagonists tamsulosin and silodosin antagonised the α1-adrenoceptor mediated vascular contractions at low doses. This suggests that these drugs will have significant effects on blood flow when given at doses used to treat benign prostatic hyperplasia and overactive bladder, and that changes in blood flow may indeed contribute to their clinical effectiveness
Original languageEnglish
Pages (from-to)98-99
Number of pages2
JournalAustralian and New Zealand Continence Journal
Volume25
Issue number4
Publication statusPublished - 2019
Event28th National Conference on Incontinence - Pullman Melbourne Albert Park, Melbourne, Australia
Duration: 13 Nov 201916 Nov 2019
Conference number: 28th
https://www.ncoi.org.au/

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tamsulosin
Overactive Urinary Bladder
Adrenergic Receptors
Urinary Bladder
Phenylephrine
Arteries
Blood Vessels
Prostatic Hyperplasia
Swine
Pharmaceutical Preparations
Urinary Bladder Neck Obstruction
Abattoirs

Cite this

@article{618752d8989241799751975a911b43da,
title = "Can the beneficial effects of tamsulosin on the overactive bladder be explained by an effect on bladder blood flow?",
abstract = "Introduction: Tamsulosin is used in the treatment of bladder outlet obstruction caused by benign prostatic hyperplasia in males. However, it has also been found to be beneficial in the treatment of overactive bladder in both men and women, although the mechanism of this action is unclear. One possible explanation could be an effect on the blood vessels supplying the bladder, where tamsulosin could potentially prevent sympathetic vasoconstriction and enhance bladder blood flow. Indeed, in recent years a number of studies have suggested that lower urinary tract dysfunction, such as overactive bladder, may be caused by reduced blood flow. The objective of this study was to examine the α1-adrenoceptors involved in contraction of the blood vessels supplying to a pig bladder (a good model of the human bladder) and investigate whether tamsulosin and silodosin at clinical doses could influence blood flow to these tissues. Materials & methods: Superior vesical artery branches from pig bladders (6-month old) were obtained from a local abattoir. Sections of artery (~4mm length, ~1mm internal diameter) were isolated and mounted between two horizontal stirrups under physiological conditions (in aerated Krebs-bicarbonate solution at 37˚C). Contractions of the circular muscle of the arteries was recorded in response to phenylephrine, a drug that acts at α1- adrenoceptors. Different subtypes of α1-adrenoceptors exist; however, in this study they were identified using selective antagonists for α1a-adrenoceptors (RS100329) and α1d- drenoceptors (BMY7378). The effects of the α1-adrenoceptor antagonist drugs tamsulosin and silodosin were also investigated. Results: The α1d-adrenoceptor antagonist BMY7378 did not affect contractions of arteries to phenylephrine. However, the α1a-adrenoceptor antagonist S100329 did significantly antagonise contractions to phenylephrine. Both antagonists, tamsulosin and silodosin, significantly antagonised contractions of arteries to phenylephrine, at low doses (Fig. 1). None of the antagonists significantly affected maximal contractions to phenylephrine. Conclusion: The results indicate that the arteries supplying blood to the bladder express the same α1- adrenoceptor subtype as those causing contraction of the human prostate. Both antagonists tamsulosin and silodosin antagonised the α1-adrenoceptor mediated vascular contractions at low doses. This suggests that these drugs will have significant effects on blood flow when given at doses used to treat benign prostatic hyperplasia and overactive bladder, and that changes in blood flow may indeed contribute to their clinical effectiveness",
author = "Damian Nilsson and Sellers, {Donna J} and Russ Chess-Williams",
year = "2019",
language = "English",
volume = "25",
pages = "98--99",
journal = "Australian and New Zealand Continence Journal",
issn = "1324-2989",
number = "4",

}

Can the beneficial effects of tamsulosin on the overactive bladder be explained by an effect on bladder blood flow? / Nilsson, Damian; Sellers, Donna J; Chess-Williams, Russ.

In: Australian and New Zealand Continence Journal, Vol. 25, No. 4, 2019, p. 98-99.

Research output: Contribution to journalMeeting AbstractResearchpeer-review

TY - JOUR

T1 - Can the beneficial effects of tamsulosin on the overactive bladder be explained by an effect on bladder blood flow?

AU - Nilsson, Damian

AU - Sellers, Donna J

AU - Chess-Williams, Russ

PY - 2019

Y1 - 2019

N2 - Introduction: Tamsulosin is used in the treatment of bladder outlet obstruction caused by benign prostatic hyperplasia in males. However, it has also been found to be beneficial in the treatment of overactive bladder in both men and women, although the mechanism of this action is unclear. One possible explanation could be an effect on the blood vessels supplying the bladder, where tamsulosin could potentially prevent sympathetic vasoconstriction and enhance bladder blood flow. Indeed, in recent years a number of studies have suggested that lower urinary tract dysfunction, such as overactive bladder, may be caused by reduced blood flow. The objective of this study was to examine the α1-adrenoceptors involved in contraction of the blood vessels supplying to a pig bladder (a good model of the human bladder) and investigate whether tamsulosin and silodosin at clinical doses could influence blood flow to these tissues. Materials & methods: Superior vesical artery branches from pig bladders (6-month old) were obtained from a local abattoir. Sections of artery (~4mm length, ~1mm internal diameter) were isolated and mounted between two horizontal stirrups under physiological conditions (in aerated Krebs-bicarbonate solution at 37˚C). Contractions of the circular muscle of the arteries was recorded in response to phenylephrine, a drug that acts at α1- adrenoceptors. Different subtypes of α1-adrenoceptors exist; however, in this study they were identified using selective antagonists for α1a-adrenoceptors (RS100329) and α1d- drenoceptors (BMY7378). The effects of the α1-adrenoceptor antagonist drugs tamsulosin and silodosin were also investigated. Results: The α1d-adrenoceptor antagonist BMY7378 did not affect contractions of arteries to phenylephrine. However, the α1a-adrenoceptor antagonist S100329 did significantly antagonise contractions to phenylephrine. Both antagonists, tamsulosin and silodosin, significantly antagonised contractions of arteries to phenylephrine, at low doses (Fig. 1). None of the antagonists significantly affected maximal contractions to phenylephrine. Conclusion: The results indicate that the arteries supplying blood to the bladder express the same α1- adrenoceptor subtype as those causing contraction of the human prostate. Both antagonists tamsulosin and silodosin antagonised the α1-adrenoceptor mediated vascular contractions at low doses. This suggests that these drugs will have significant effects on blood flow when given at doses used to treat benign prostatic hyperplasia and overactive bladder, and that changes in blood flow may indeed contribute to their clinical effectiveness

AB - Introduction: Tamsulosin is used in the treatment of bladder outlet obstruction caused by benign prostatic hyperplasia in males. However, it has also been found to be beneficial in the treatment of overactive bladder in both men and women, although the mechanism of this action is unclear. One possible explanation could be an effect on the blood vessels supplying the bladder, where tamsulosin could potentially prevent sympathetic vasoconstriction and enhance bladder blood flow. Indeed, in recent years a number of studies have suggested that lower urinary tract dysfunction, such as overactive bladder, may be caused by reduced blood flow. The objective of this study was to examine the α1-adrenoceptors involved in contraction of the blood vessels supplying to a pig bladder (a good model of the human bladder) and investigate whether tamsulosin and silodosin at clinical doses could influence blood flow to these tissues. Materials & methods: Superior vesical artery branches from pig bladders (6-month old) were obtained from a local abattoir. Sections of artery (~4mm length, ~1mm internal diameter) were isolated and mounted between two horizontal stirrups under physiological conditions (in aerated Krebs-bicarbonate solution at 37˚C). Contractions of the circular muscle of the arteries was recorded in response to phenylephrine, a drug that acts at α1- adrenoceptors. Different subtypes of α1-adrenoceptors exist; however, in this study they were identified using selective antagonists for α1a-adrenoceptors (RS100329) and α1d- drenoceptors (BMY7378). The effects of the α1-adrenoceptor antagonist drugs tamsulosin and silodosin were also investigated. Results: The α1d-adrenoceptor antagonist BMY7378 did not affect contractions of arteries to phenylephrine. However, the α1a-adrenoceptor antagonist S100329 did significantly antagonise contractions to phenylephrine. Both antagonists, tamsulosin and silodosin, significantly antagonised contractions of arteries to phenylephrine, at low doses (Fig. 1). None of the antagonists significantly affected maximal contractions to phenylephrine. Conclusion: The results indicate that the arteries supplying blood to the bladder express the same α1- adrenoceptor subtype as those causing contraction of the human prostate. Both antagonists tamsulosin and silodosin antagonised the α1-adrenoceptor mediated vascular contractions at low doses. This suggests that these drugs will have significant effects on blood flow when given at doses used to treat benign prostatic hyperplasia and overactive bladder, and that changes in blood flow may indeed contribute to their clinical effectiveness

M3 - Meeting Abstract

VL - 25

SP - 98

EP - 99

JO - Australian and New Zealand Continence Journal

JF - Australian and New Zealand Continence Journal

SN - 1324-2989

IS - 4

ER -