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A possible role of decreased relaxation mediated by β‐adrenoceptors in bladder outlet obstruction by benign prostatic hyperplasia
Author(s) -
Tsujii Toshihiko,
Azuma Hiroshi,
Yamaguchi Tomohiro,
Oshima Hiroyuki
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14527.x
Subject(s) - hyperplasia , chemistry , endocrinology , contraction (grammar) , prazosin , medicine , prostate , detrusor muscle , stimulation , forskolin , urinary bladder , isoprenaline , receptor , antagonist , cancer
1 To explore mechanisms of urinary obstruction in benign prostatic hyperplasia (BPH), the features of contraction and relaxation in human hyperplastic and non‐hyperplastic (control) prostatic tissues were investigated for β‐ and α 1 ‐adrenoceptors by radioligand binding and in vitro isometric tension experiments. 2 Hyperplastic and control prostatic tissues had a similar number (per mg protein) of prazosin binding sites with similar affinities. Noradrenaline (NA) induced dose‐dependent contraction in both tissues. Contraction induced by either exogenous NA or transmural stimulation was inhibited by prazosin in both tissues, indicating that the same contractile mechanisms mediated by α 1 ‐adrenoceptors exist in hyperplastic and control tissues. 3 The number of dihydroalprenolol (DHA) binding sites (per mg protein) was less in hyperplastic tissues than in controls, whereas the affinity to the ligand was identical in both tissues. Isoprenaline caused a marked relaxation of the tonic contraction induced by KCl in control tissues, but not in hyperplastic tissues. Propranolol enhanced exogenous NA‐ or transmural stimulation‐induced contraction more in control tissues than in hyperplastic tissues. Both tissues, however, similarly responded to forskolin by relaxation. 4 These results indicate that decreased β‐adrenoceptor‐mediated relaxation in hyperplastic prostatic tissues, which is attributable at least in part to the decreased number of β‐adrenoceptors, may play a role in the urinary obstruction of BPH in addition to mechanical compression of the urethra by the enlarged prostate.