In vivo rat model to measure hypogastric nerve stimulation-induced seminal vesicle and vasal pressure responses simultaneously

Abstract

This study presents a modified in vivo model in which the intraluminal pressures of the seminal vesicle and vas deferens can be measured simultaneously. Male Sprague-Dawley rats were grouped based on agent administered: serotonin, clomipramine, fluoxetine, sertraline, paroxetine, prazosin, terazosin, and tamsulosin. The control responses to hypogastric nerve stimulation (HNS) were recorded in each animal, and HNS was repeated after each drug administration. Serotonergic agents resulted in concentration-dependent inhibition of the HNS-induced seminal vesicle pressure increases (clomipramine4serotonin4fluoxetine4sertralineEparoxetine). On the other hand, only serotonin and clomipramine significantly inhibited vasal pressure responses. a-Adrenergic blockers inhibited both intraluminal pressure responses in a concentration-dependent manner. This model illustrates the importance of the hypogastric nerve for the stimulation of the seminal tract, with attention focused on the seminal vesicle. This model may be useful for the evaluation of drugs for the treatment of premature ejaculation.

A Role for Peripheral 5-HT2 Receptors in Serotonin-Induced Facilitation of the Expulsion Phase of Ejaculation in Male Rats

“…Previous studies suggest that activation of 5‐HT 1A receptors in the brain and spinal cord contribute to a facilitation of sexual behavior, while activation of 5‐HT 1B and 5‐HT 2C receptors contribute to the inhibition of sexual behavior [18,19,22,42–45]. In the periphery, 5‐HT is thought to be involved in the inhibition of secretion of seminal fluids into the urethra, by inhibiting the ability of sympathetic nerve stimulation to produce contractions of the seminal vesicle and vas deferens [46–48]. In human tissue studies, 5‐HT and SSRIs inhibit the seminal vesicle smooth muscle contractions induced by norepinephrine [49].…”

“…The thick horizontal bar indicates the occlusion period or latency to first burst. UPP = urethral perfusion pressure inhibiting the ability of sympathetic nerve stimulation to produce contractions of the seminal vesicle and vas deferens [46][47][48]. In human tissue studies, 5-HT and SSRIs inhibit the seminal vesicle smooth muscle contractions induced by norepinephrine [49].…”

Dapoxetine for Premature Ejaculation

“… 13 Later studies demonstrated significantly inhibited increases in seminal vesicle pressure induced by hypogastric nerve stimulation, having the effect of prolonging ejaculatory latency by inhibiting intraluminal pressure increases in the seminal vesicles. 14 Because seminal vesicles produce a greater amount of ejaculate than the vas deferens, the discovery of this inhibitory effect proved to be important. The proposed pathogenesis of PE is an imbalance between hypersensitive responses at the 5HT 1A receptor and hyposensitive responses at the 5HT 1B or 5HT 2C receptors, leading to decreased ejaculatory latency due to either inappropriate levels of 5HT or altered sensitivity of its receptors.…”

Effects of Tamsulosin on Premature Ejaculation in Men with Benign Prostatic Hyperplasia

“…However, their report was inconsistent with the result of a previous study, showing that tamsulosin-induced ED was attributable to retrograde ejaculation that was caused by the relaxation of the smooth muscle in the prostatic urethra and the bladder outlet. Kim et al [18] reported that the internal pressure of the seminal vesicle or vas deferens upon ejaculation decreased in rats compared with the control group after the administration of an a1-adrenoreceptor antagonist. Tamsulosin-induced ED may occur as a negative effect in normal subjects, but it can help ejaculation delay in patients with PE.…”