1983 Volume 74 Issue 12 Pages 2054-2069
Strips of the prostatic hyperplastic nodules were studied by observing the mechanical response to application of certain drugs. Phenylephrine in doses over 5×10-7g/ml produced contraction which was abolished following treatment with phentolamine or prazosin. Adiministration of PGF2α(>5×10-7g/ml) also produced contraction, however, neither phentolamine nor atropine inhibited the PGF2α-induced contraction. Low concentrations (10-8-10-7g/ml) of PGE2 inhibited the spontaneously generated contraction while high concentrations (10-6g/ml) produced a slight contraction. Administration of acetylcholine or isoproterenol to the muscle bath produced no response.
The small hyperplastic nodules showed a higher sensitivity to phenylephrine. Sensitivity to the PGs, however, was independent from the size of nodules.
The sensitivity to KCl, phenylephrine and PGs was about double that seen in case of the normal prostate tissues. Neural elements distributed in the hyperplastic nodules were fewer than in the normal prostate. Furthermore, in smooth muscle, the main component of hyperplastic nodules was estimated from the mechanical response and also from histological observations. The dense distribution of α-adrenergic receptor on the smooth muscle cell membrane of hyperplastic nodules was also evident.
In patients with benign prostatic hypertrophy, the urethral pressure profile in cases of acute urinary retention could be estimated from the high prostatic pressure and reduced length of the prostatic adenoma. Administration of prazosin produced a remarkable decrease in the prostatic pressure observed from the urethral pressure profile, and the clinical effects were excellent. Therefore, acute urinary retention in patients with benign prostatic hypertrophy probably is related to the contraction of smooth muscle cells in the hyperplastic nodule following activation of the α-adrenergic receptors.