The effects of α1A-adrenoceptor antagonists on the urethral perfusion pressure of the female rat

Jae Hyun Bae, Phil Bum Jung, Jeong Gu Lee

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

OBJECTIVE: To assess the effects of α1A-adrenoceptor antagonists on urethral perfusion pressure (UPP) in the female rate and their therapeutic potential for treating female bladder outlet obstruction (BOO). MATERIALS AND METHODS: A cannula was inserted into the femoral arteries of female rats to administer tamsulosin (group I), doxazosin (group II) or phentolamine (group III) and to monitor systemic blood pressure. Tamsulosin was also administered to male rats (group IV). UPP and vesical pressures (Pves) were monitored using a triple-lumen catheter. RESULTS: After administration of tamsulosin to group I the frequency of bladder contractions decreased significantly and the duration of minimal urethral relaxation with high-frequency oscillations (HFOs) was significantly prolonged. Except for mean arterial blood pressure (MAP), none of the variables in group I differed significantly from those in group II and group III. The change in MAP after tamsulosin treatment was significantly lower than after doxazosin or phentolamine. Except for the maximum Pves, which was significantly higher in males (group IV) than in females of group I, the UPP and Pves curves of male rats were similar to those of females before giving tamsulosin. The prolonged frequency and duration of HFO in group IV (with tamsulosin) were significantly different from those of females. CONCLUSIONS: The α1A- adrenergic receptor may be a functional subtype in the female rat urethra. α1A-adrenoceptor antagonists prolonged the duration of HFOs and decreased the frequency of involuntary bladder contraction. It is possible that treatment with α1A-adrenoceptor antagonists would not only improve obstructive symptoms, but also ameliorate irritative symptoms by prolonging HFOs and the frequency of involuntary bladder contractions.

Original languageEnglish
Pages (from-to)1131-1135
Number of pages5
JournalBJU International
Volume96
Issue number7
DOIs
Publication statusPublished - 2005 Nov 1

Fingerprint

tamsulosin
Adrenergic Receptors
Perfusion
Pressure
Doxazosin
Phentolamine
Arterial Pressure
Urinary Bladder
Blood Pressure Monitors
Urinary Bladder Neck Obstruction
Urethra
Femoral Artery
Catheters

Keywords

  • α-adrenoceptor antagonist
  • Tamsulosin
  • Urethral perfusion pressure

ASJC Scopus subject areas

  • Urology

Cite this

The effects of α1A-adrenoceptor antagonists on the urethral perfusion pressure of the female rat. / Bae, Jae Hyun; Jung, Phil Bum; Lee, Jeong Gu.

In: BJU International, Vol. 96, No. 7, 01.11.2005, p. 1131-1135.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVE: To assess the effects of α1A-adrenoceptor antagonists on urethral perfusion pressure (UPP) in the female rate and their therapeutic potential for treating female bladder outlet obstruction (BOO). MATERIALS AND METHODS: A cannula was inserted into the femoral arteries of female rats to administer tamsulosin (group I), doxazosin (group II) or phentolamine (group III) and to monitor systemic blood pressure. Tamsulosin was also administered to male rats (group IV). UPP and vesical pressures (Pves) were monitored using a triple-lumen catheter. RESULTS: After administration of tamsulosin to group I the frequency of bladder contractions decreased significantly and the duration of minimal urethral relaxation with high-frequency oscillations (HFOs) was significantly prolonged. Except for mean arterial blood pressure (MAP), none of the variables in group I differed significantly from those in group II and group III. The change in MAP after tamsulosin treatment was significantly lower than after doxazosin or phentolamine. Except for the maximum Pves, which was significantly higher in males (group IV) than in females of group I, the UPP and Pves curves of male rats were similar to those of females before giving tamsulosin. The prolonged frequency and duration of HFO in group IV (with tamsulosin) were significantly different from those of females. CONCLUSIONS: The α1A- adrenergic receptor may be a functional subtype in the female rat urethra. α1A-adrenoceptor antagonists prolonged the duration of HFOs and decreased the frequency of involuntary bladder contraction. It is possible that treatment with α1A-adrenoceptor antagonists would not only improve obstructive symptoms, but also ameliorate irritative symptoms by prolonging HFOs and the frequency of involuntary bladder contractions.",
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N2 - OBJECTIVE: To assess the effects of α1A-adrenoceptor antagonists on urethral perfusion pressure (UPP) in the female rate and their therapeutic potential for treating female bladder outlet obstruction (BOO). MATERIALS AND METHODS: A cannula was inserted into the femoral arteries of female rats to administer tamsulosin (group I), doxazosin (group II) or phentolamine (group III) and to monitor systemic blood pressure. Tamsulosin was also administered to male rats (group IV). UPP and vesical pressures (Pves) were monitored using a triple-lumen catheter. RESULTS: After administration of tamsulosin to group I the frequency of bladder contractions decreased significantly and the duration of minimal urethral relaxation with high-frequency oscillations (HFOs) was significantly prolonged. Except for mean arterial blood pressure (MAP), none of the variables in group I differed significantly from those in group II and group III. The change in MAP after tamsulosin treatment was significantly lower than after doxazosin or phentolamine. Except for the maximum Pves, which was significantly higher in males (group IV) than in females of group I, the UPP and Pves curves of male rats were similar to those of females before giving tamsulosin. The prolonged frequency and duration of HFO in group IV (with tamsulosin) were significantly different from those of females. CONCLUSIONS: The α1A- adrenergic receptor may be a functional subtype in the female rat urethra. α1A-adrenoceptor antagonists prolonged the duration of HFOs and decreased the frequency of involuntary bladder contraction. It is possible that treatment with α1A-adrenoceptor antagonists would not only improve obstructive symptoms, but also ameliorate irritative symptoms by prolonging HFOs and the frequency of involuntary bladder contractions.

AB - OBJECTIVE: To assess the effects of α1A-adrenoceptor antagonists on urethral perfusion pressure (UPP) in the female rate and their therapeutic potential for treating female bladder outlet obstruction (BOO). MATERIALS AND METHODS: A cannula was inserted into the femoral arteries of female rats to administer tamsulosin (group I), doxazosin (group II) or phentolamine (group III) and to monitor systemic blood pressure. Tamsulosin was also administered to male rats (group IV). UPP and vesical pressures (Pves) were monitored using a triple-lumen catheter. RESULTS: After administration of tamsulosin to group I the frequency of bladder contractions decreased significantly and the duration of minimal urethral relaxation with high-frequency oscillations (HFOs) was significantly prolonged. Except for mean arterial blood pressure (MAP), none of the variables in group I differed significantly from those in group II and group III. The change in MAP after tamsulosin treatment was significantly lower than after doxazosin or phentolamine. Except for the maximum Pves, which was significantly higher in males (group IV) than in females of group I, the UPP and Pves curves of male rats were similar to those of females before giving tamsulosin. The prolonged frequency and duration of HFO in group IV (with tamsulosin) were significantly different from those of females. CONCLUSIONS: The α1A- adrenergic receptor may be a functional subtype in the female rat urethra. α1A-adrenoceptor antagonists prolonged the duration of HFOs and decreased the frequency of involuntary bladder contraction. It is possible that treatment with α1A-adrenoceptor antagonists would not only improve obstructive symptoms, but also ameliorate irritative symptoms by prolonging HFOs and the frequency of involuntary bladder contractions.

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