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Characterization of α 1 ‐adrenoceptor subtypes in tension response of human prostate to electrical field stimulation
Author(s) -
Guh JihHwa,
Chueh ShihChieh,
Ko FengNien,
Teng CheMing
Publication year - 1995
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.1476-5381.1995.tb16331.x
Subject(s) - prazosin , vas deferens , endocrinology , medicine , stimulation , urapidil , prostate , phenylephrine , chemistry , nifedipine , contraction (grammar) , biology , antagonist , receptor , calcium , cancer , blood pressure , heart rate
1 The effects of various α 1 ‐adrenoceptor antagonists and nifedipine on tension responses of human prostate to electrical field stimulation were evaluated in this study. 2 Prazosin (3 × 10 −10 to 10 −8 M ) and 5‐methyl‐urapidil (10 −9 to 3 × 10 −8 M ) blocked concentration‐dependently the tension responses to electrical field stimulation and completely abolished them in the maximal concentrations (10 −8 M and 3 × 10 −8 M , respectively); in contrast, chloroethylclonidine (CEC), in the maximal concentration of 100 μ M , blocked these effects by only 50%. 3 The contractile responses of rat vas deferens and spleen to exogenously‐applied α 1r adrenoceptor agonists were competitively inhibited by prazosin and 5‐methyl‐urapidil; in addition, the pA 2 values were calculated and the relative potencies with reference to prazosin were obtained. The relative potency of 5‐methyl‐urapidil in human prostate (0.105) was close to that in rat vas deferens (0.257), which contains primarily putative α 1A ‐adrenoceptors. However, it was much more than that in rat spleen (0.011), which contains primarily putative α 1B ‐adrenoceptors. 4 Nifedipine (10 −8 to 10 −6 M ) inhibited concentration‐dependently the contractile responses to electrical field stimulation in human prostate; in addition, the inhibition percentages were similar to those to exogenously‐applied noradrenaline in rat vas deferens. In contrast, CEC (10 μ M ), which almost flattened the concentration‐response curve of the rat spleen to phenylephrine, only partially inhibited (by 33.1%) the nerve‐mediated contraction of human prostate. 5 The involvement of prejunctional α 2 ‐adrenoceptors situated on the sympathetic nerve terminals of human prostate was also examined. Clonidine (3 × 10 −9 to 3 × 10 −7 M ) blocked concentration‐dependently the contractile response to electrical field stimulation of human prostate and this inhibitory effect was reversed by yohimbine (10 −7 M ). Additionally, the inhibitory effect of CEC (3 × 10 −6 to 3 × 10 −4 M ) to the nerve‐mediated contraction was also partially reversed by yohimbine (10 −7 M ). 6 It is suggested that the putative α 1A ‐adrenoceptors in human prostate may be functionally confined to the synaptic region whereas only minor populations of the putative α 1B ‐ and/or α lc ‐adrenoceptors exist in this region.

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