{'fraction_non_alphanumeric': 0.0436046511627907, 'fraction_numerical': 0.03737541528239203, 'mean_word_length': 5.729050279329609, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Characterization of α1‐adrenoceptor subtypes in tension response of human prostate to electrical field stimulation

1 The effects of various α1‐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 10−8M) 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 μM, blocked these effects by only 50%. 3 The contractile responses of rat vas deferens and spleen to exogenously‐applied α1radrenoceptor agonists were competitively inhibited by prazosin and 5‐methyl‐urapidil; in addition, the pA2 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 α1A‐adrenoceptors. However, it was much more than that in rat spleen (0.011), which contains primarily putative α1B‐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 μM), 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 α2‐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 (10−7M). 6 It is suggested that the putative α1A‐adrenoceptors in human prostate may be functionally confined to the synaptic region whereas only minor populations of the putative α1B‐ and/or αlc‐adrenoceptors exist in this region.