Testosterone-induced prostatic growth in the rat causes bladder overactivity unrelated to detrusor hypertrophy

Raj Kumar Pandita, Katarina Persson, Petter Hedlund, Karl Erik Andersson

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

BACKGROUND. Testosterone treatment of rats produces prostatic hypertrophy and detrusor overactivity. Whether or not the detrusor overactivity can be related to an increase in the responsiveness of lower urinary tract smooth muscles is not known. METHODS. Male Sprague-Dawley rats were given daily injections of testosterone propionate for 2 weeks. Effects on cystometric parameters and on the responsiveness of isolated detrusor, urethral, and prostate smooth muscle preparations to drugs and electrical field stimulation were investigated. RESULTS. Testosterone treatment increased prostatic weight twofold (controls, 768 mg; testosterone-treated, 1,478 mg), but not bladder weight (103 mg vs. 116 mg). Micturition pressure (77%), bladder capacity (75%), residual volume (56%), and micturition volume (83%) increased significantly in treated animals, and bladder overactivity developed. No effect of intraarterial doxazosin on these changes was observed. The differences in urodynamic parameters between control and testosterone-treated rats could not be correlated with changes in bladder, urethral, or prostate excitatory innervation, as revealed by responses to electrical field stimulation, or by smooth muscle responses to different contractant drugs. CONCLUSIONS. Some of the urodynamic effects seen after testosterone treatment seem to be caused by the mechanical obstruction of the enlarged prostate. Since there were no changes in smooth muscle responsiveness, it is suggested that the bladder overactivity observed can partly be related to testosterone-induced changes of the micturition reflex at the lower urinary tract, spinal, and/or supraspinal levels.

Original languageEnglish
Pages (from-to)102-108
Number of pages7
JournalProstate
Volume35
Issue number2
DOIs
Publication statusPublished - May 1 1998

Fingerprint

Hypertrophy
Testosterone
Urinary Bladder
Smooth Muscle
Urination
Growth
Prostate
Urodynamics
Urinary Tract
Electric Stimulation
Doxazosin
Testosterone Propionate
Weights and Measures
Drug Compounding
Residual Volume
Prostatic Hyperplasia
Sprague Dawley Rats
Reflex
Therapeutics
Pressure

Keywords

  • Cystometry
  • Electrical field stimulation
  • Micturition
  • Outflow obstruction

ASJC Scopus subject areas

  • Urology

Cite this

Testosterone-induced prostatic growth in the rat causes bladder overactivity unrelated to detrusor hypertrophy. / Pandita, Raj Kumar; Persson, Katarina; Hedlund, Petter; Andersson, Karl Erik.

In: Prostate, Vol. 35, No. 2, 01.05.1998, p. 102-108.

Research output: Contribution to journalArticle

Pandita, Raj Kumar ; Persson, Katarina ; Hedlund, Petter ; Andersson, Karl Erik. / Testosterone-induced prostatic growth in the rat causes bladder overactivity unrelated to detrusor hypertrophy. In: Prostate. 1998 ; Vol. 35, No. 2. pp. 102-108.
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N2 - BACKGROUND. Testosterone treatment of rats produces prostatic hypertrophy and detrusor overactivity. Whether or not the detrusor overactivity can be related to an increase in the responsiveness of lower urinary tract smooth muscles is not known. METHODS. Male Sprague-Dawley rats were given daily injections of testosterone propionate for 2 weeks. Effects on cystometric parameters and on the responsiveness of isolated detrusor, urethral, and prostate smooth muscle preparations to drugs and electrical field stimulation were investigated. RESULTS. Testosterone treatment increased prostatic weight twofold (controls, 768 mg; testosterone-treated, 1,478 mg), but not bladder weight (103 mg vs. 116 mg). Micturition pressure (77%), bladder capacity (75%), residual volume (56%), and micturition volume (83%) increased significantly in treated animals, and bladder overactivity developed. No effect of intraarterial doxazosin on these changes was observed. The differences in urodynamic parameters between control and testosterone-treated rats could not be correlated with changes in bladder, urethral, or prostate excitatory innervation, as revealed by responses to electrical field stimulation, or by smooth muscle responses to different contractant drugs. CONCLUSIONS. Some of the urodynamic effects seen after testosterone treatment seem to be caused by the mechanical obstruction of the enlarged prostate. Since there were no changes in smooth muscle responsiveness, it is suggested that the bladder overactivity observed can partly be related to testosterone-induced changes of the micturition reflex at the lower urinary tract, spinal, and/or supraspinal levels.

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