Amobi N I, Smith I C
Biomedical Sciences Division, King's College London, UK.
J Reprod Fertil. 1992 May;95(1):1-10. doi: 10.1530/jrf.0.0950001.
Thioridazine (0.1-10 mumol l-1) inhibited shortening of specimens of human vasa deferentia induced by noradrenaline (100 mumol l-1) or high extracellular potassium (136 mmol l-1). Thioridazine did not inhibit the lengthening response. In Ca(2+)-free media with EGTA (0.5 mmol l-1) similar results were obtained with responses to noradrenaline, but exposure to potassium elicited small contractions that were potentiated by thioridazine. Both shortening and lengthening responses to noradrenaline were antagonized by the alpha-adrenoceptor blockers prazosin (1-10 mumol l-1) and phentolamine (1-10 mumol l-1) and by the Ca2+ antagonists verapamil (10 mumol l-1) and diltiazem (10 mumol l-1). Responses to potassium were virtually abolished by the Ca2+ antagonists. These results show that thioridazine specifically inhibits longitudinal muscle of the human vas deferens and that its action cannot be entirely accounted for by a blockade of voltage-gated Ca2+ channels.
硫利达嗪(0.1 - 10 μmol l⁻¹)抑制去甲肾上腺素(100 μmol l⁻¹)或高细胞外钾(136 mmol l⁻¹)诱导的人输精管标本缩短。硫利达嗪不抑制延长反应。在含有乙二醇双(2-氨基乙基醚)四乙酸(EGTA,0.5 mmol l⁻¹)的无钙培养基中,对去甲肾上腺素的反应得到类似结果,但暴露于钾会引发小的收缩,硫利达嗪可增强这种收缩。对去甲肾上腺素的缩短和延长反应均被α-肾上腺素能受体阻滞剂哌唑嗪(1 - 10 μmol l⁻¹)和酚妥拉明(1 - 10 μmol l⁻¹)以及钙拮抗剂维拉帕米(10 μmol l⁻¹)和地尔硫䓬(10 μmol l⁻¹)拮抗。对钾的反应几乎被钙拮抗剂消除。这些结果表明,硫利达嗪特异性抑制人输精管的纵行肌,其作用不能完全由电压门控钙通道的阻断来解释。