Department of Pharmacology, Universidade Estadual Paulista, Botucatu, SP, Brazil.
J Sex Med. 2012 Jan;9(1):159-68. doi: 10.1111/j.1743-6109.2011.02410.x. Epub 2011 Aug 2.
Premature ejaculation is one of the most common male sexual dysfunctions. Current pharmacological treatments involve reduction in penile sensitivity by local anesthetics or increase of ejaculatory threshold by selective serotonin reuptake inhibitors. α1-Adrenoceptors (α1-ARs) and L-type calcium channels are expressed in the smooth muscles of the male reproductive tract, and their activations play an important role in the physiological events involved in the seminal emission phase of ejaculation.
To evaluate if the inhibition of the contractility of the vas deferens and seminal vesicle by α1-AR antagonism or the L-type calcium channel blockade can delay ejaculation.
The effects of the α1-AR antagonist tamsulosin and of the L-type calcium channel blockers, nifedipine and (S)-(+)-niguldipine, on contractions induced by norepinephrine in the rat vas deferens and seminal vesicles in vitro and on the ejaculation latency of male rats in behavioral mating tests were evaluated.
Tension development of vas deferens and seminal vesicles in response to norepinephrine in vitro and behavioral mating parameters were quantified.
Tension development of vas deferens and seminal vesicle to α1-AR activation was significantly inhibited by tamsulosin, nifedipine, and (S)-(+)-niguldipine. Tamsulosin displayed insurmountable antagonism of contractions induced by norepinephrine in the rat vas deferens and seminal vesicle. Ejaculation latency of male rats was not modified by tamsulosin, nifedipine, or (S)-(+)-niguldipine; however, both the number and weight of the seminal plugs recovered from female rats mated with male rats treated with tamsulosin were significantly reduced.
Seminal emission impairment by inhibition of vas deferens or seminal vesicle contractility by L-type calcium channel blockade or α1-AR antagonism is not able to delay the ejaculation.
早泄是男性最常见的性功能障碍之一。目前的药物治疗方法包括局部麻醉剂降低阴茎敏感度或选择性 5-羟色胺再摄取抑制剂增加射精阈值。α1-肾上腺素能受体（α1-AR）和 L 型钙通道在男性生殖道平滑肌中表达，其激活在射精的精液排放阶段涉及的生理事件中发挥重要作用。
评估 α1-AR 拮抗或 L 型钙通道阻断对输精管和精囊收缩的抑制是否能延迟射精。
评估α1-AR 拮抗剂坦索罗辛和 L 型钙通道阻滞剂硝苯地平及（S）-（+）-尼群地平对大鼠输精管和精囊体外去甲肾上腺素诱导收缩的影响，以及对雄性大鼠性行为交配试验中射精潜伏期的影响。
体外去甲肾上腺素诱导的输精管和精囊张力发展以及性行为交配参数的定量。
坦索罗辛、硝苯地平和（S）-（+）-尼群地平显著抑制输精管和精囊对 α1-AR 激活的张力发展。坦索罗辛对大鼠输精管和精囊去甲肾上腺素诱导的收缩显示出不可逾越的拮抗作用。坦索罗辛、硝苯地平和（S）-（+）-尼群地平均未改变雄性大鼠的射精潜伏期；然而，与未接受治疗的雄性大鼠相比，接受坦索罗辛治疗的雄性大鼠与雌性大鼠交配后，从雌性大鼠中回收的精液栓的数量和重量明显减少。
通过抑制输精管或精囊收缩来抑制 L 型钙通道或 α1-AR 拮抗作用来损害精液排放，不能延迟射精。
