Teng C M, Guh J H, Ko F N
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei.
Eur J Pharmacol. 1994 Nov 14;265(1-2):61-6. doi: 10.1016/0014-2999(94)90223-2.
The effects of some alpha 1-adrenoceptor antagonists (prazosin, nonselective for the alpha 1A- and alpha 1B-adrenoceptor subtypes; 5-methyl-urapidil, selective for the alpha 1A-adrenoceptor subtype; chloroethylclonidine, selective for the alpha 1B-adrenoceptor subtype) and nifedipine were compared on contractile responses to noradrenaline or phenylephrine in human prostatic tissues, rat vas deferens and spleen. In rat vas deferens, nifedipine (1 microM), but not chloroethylclonidine (100 microM), almost completely abolished noradrenaline-induced contraction, the pA2 values for prazosin and 5-methyl-urapidil against noradrenaline being 9.29 and 8.55, respectively. In rat spleen, chloroethylclonidine reduced (by 57%) the maximum contraction induced by phenylephrine; nifedipine was ineffective. The log concentration-response curve was shifted significantly to the right; the pA2 values of prazosin and 5-methyl-urapidil against phenylephrine were 9.45 and 7.21, respectively. In human prostatic tissues, both nifedipine and chloroethylclonidine produced significant inhibition of noradrenaline-induced contractions. Chloroethylclonidine produced a 44% reduction of the maximum contraction to noradrenaline and shifted the log concentration-response curve to the right. In contrast, nifedipine, while reducing the maximum response to a similar extent, produced a small rightward shift in the log concentration-response curve. The pA2 values for prazosin and 5-methyl-urapidil against noradrenaline were 9.21 and 7.74, respectively. The pA2 values for prazosin in these three tissues did not vary significantly, whereas that for 5-methyl-urapidil in human prostatic tissue was intermediate between that in rat vas deferens and that in rat spleen: these tissues contain primarily alpha 1A- and alpha 1B-adrenoceptor subtypes, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
比较了一些α1肾上腺素能受体拮抗剂（哌唑嗪，对α1A和α1B肾上腺素能受体亚型无选择性；5-甲基乌拉地尔，对α1A肾上腺素能受体亚型有选择性；氯乙可乐定，对α1B肾上腺素能受体亚型有选择性）和硝苯地平对人前列腺组织、大鼠输精管和脾脏中去甲肾上腺素或去氧肾上腺素收缩反应的影响。在大鼠输精管中，硝苯地平（1微摩尔）几乎完全消除了去甲肾上腺素诱导的收缩，而氯乙可乐定（100微摩尔）则无此作用，哌唑嗪和5-甲基乌拉地尔对去甲肾上腺素的pA2值分别为9.29和8.55。在大鼠脾脏中，氯乙可乐定使去氧肾上腺素诱导的最大收缩降低了57%；硝苯地平无效。对数浓度-反应曲线显著右移；哌唑嗪和5-甲基乌拉地尔对去氧肾上腺素的pA2值分别为9.45和7.21。在人前列腺组织中，硝苯地平和氯乙可乐定都显著抑制了去甲肾上腺素诱导的收缩。氯乙可乐定使对去甲肾上腺素的最大收缩降低了44%，并使对数浓度-反应曲线右移。相比之下，硝苯地平虽然使最大反应降低了类似程度，但对数浓度-反应曲线右移较小。哌唑嗪和5-甲基乌拉地尔对去甲肾上腺素的pA2值分别为9.21和7.74。这三种组织中哌唑嗪的pA2值无显著差异，而人前列腺组织中5-甲基乌拉地尔的pA2值介于大鼠输精管和大鼠脾脏之间：这些组织分别主要含有α1A和α1B肾上腺素能受体亚型。（摘要截短至250字）
