Characterization of the Effects of Various Drugs Likely to Affect Smooth Muscle Tension on Isolated Human Seminal Vesicle Tissue

Birowo, Ponco; Ückert, Stefan; Kedia, George T.; Sonnenberg, Joachim; Thon, W. F.; Rahardjo, Djoko; Kuczyk, Markus A.

doi:10.1016/j.urology.2009.09.034

Cited by 18 publications

(11 citation statements)

References 25 publications

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“…Interestingly, the contractions induced by norepinephrine in the vas deferens were completely abolished by nifedipine and (S)‐(+)‐niguldipine, whereas in the rat seminal vesicle, approximately 30% of the contraction in response to norepinephrine remained in the presence of these two dihydropyridine‐calcium channel blockers. Similarly to what was found in the present study, a significant part of the contractions of guinea pig and human seminal vesicles in response to norepinephrine is reported to be resistant to dihydropyridine‐calcium channel blockers, indicating that calcium mobilization from intracellular stores and/or extracellular calcium influx through non‐L‐type calcium channels contribute to the contractions induced by α 1 ‐AR activation in this tissue [29,30].…”

Section: Discussionsupporting

confidence: 88%

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Kiguti

Pupo

2012

The Journal of Sexual Medicine

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Introduction 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. Aim 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. Methods 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. Main Outcome Measure Tension development of vas deferens and seminal vesicles in response to norepinephrine in vitro and behavioral mating parameters were quantified. Results 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. Conclusion 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.

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Section: Discussionsupporting

confidence: 88%

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Kiguti

Pupo

2012

The Journal of Sexual Medicine

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“…Ejaculation commonly consists of two successive processes of emission and expulsion (Giuliano, 2011). The emission is characterized by the secretion of seminal fluids from the accessory sex gland and the closure of the bladder neck, and this phase is mainly activated by sympathetic neurons (Birowo et al, 2010). However, expulsion is the process of propelling spermatozoa from the prostatic urethra to the urethral meatus induced by rhythmic contractions of perineal striated muscles, which depend on the somatomotor system (Giuliano, 2011).…”

Section: Discussionmentioning

confidence: 99%

Centrally mediated ejaculatory response via sympathetic outflow in rats: role of N‐methyl‐D‐aspartic acid receptors in paraventricular nucleus

et al. 2016

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SUMMARYEjaculation is mediated by a spinal generator, which integrates inputs related to the sexual activity and coordinates sympathetic, parasympathetic, and motor outflow. Previous clinical studies indicate that primary premature ejaculation is related to the hyperactivity of the sympathetic nervous system. In this study, we explored the roles of N-methyl-D-aspartic acid (NMDA) receptors in paraventricular nucleus of the hypothalamus (PVN) on ejaculatory responses and its potential mechanism in the rats. We found that microinjection of 0.20 nmol NMDA into the PVN reduced the latency of intromission and facilitated ejaculation during copulation. Moreover, delayed ejaculation and intromission were observed after the rats were microinjected with NMDA receptor antagonist D (À)-2-Amino-5-phosphonopentanoic acid (AP-5). However, we discovered that microinjection of NMDA into PVN significantly increased baseline lumbar splanchnic nerve activity (LSNA), and the NMDA dose was positively correlated with the increased LSNA (r = 0.875, p = 0.04). Meanwhile, the plasma norepinephrine level in rats injected with NMDA was much higher than that in rats injected with saline (1453.4 AE 136.4 pg/mL vs. 492.3 AE 36.8 pg/mL, p < 0.01). Additionally, AP-5 reduced the baseline LSNA and abrogated the enhancing activity of NMDA in LSNA. Thus, we propose that NMDA receptors in PVN may facilitate ejaculation through enhancing the activity of sympathetic system.

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“…Of these ejaculatory disorders, pre‐mature ejaculation, retrograde ejaculation and anejaculation are common problems of male sexual medicine (Aschka et al ., ; Hatzimouratidis et al ., ). The emission stage, through sympathetically mediated neurons, leads to the contractions of the seminal vesicles (SV) and the prostate, with expulsion of spermatozoa and seminal fluid into the posterior urethra (Birowo et al ., ). The SV is a secretomotor organ, which is composed of outer smooth muscle layer and subepithelial glandular tissue.…”

Section: Introductionmentioning

confidence: 97%

The role of sympathetic and parasympathetic nerve systems on the smooth muscle of rat seminal vesicles – experimental results and speculation for physiological implication on ejaculation

Hsieh

Chang

et al. 2013

Andrology

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SUMMARYEjaculation is a process involving sympathetic and parasympathetic effects during different stages -emission and ejection. Some conditions of ejaculation dysfunction are associated with autonomic nerves. However, the exact effects of autonomic nerves on ejaculation are not well defined. Autonomic agonists induce different recorded trace patterns of seminal vesicular contraction. The different traces contain different components of phasic and tonic contraction, which may have physiological implications. In this study, we examined isolated rat seminal vesicle (SV) contraction by phenylephrine (PE), acetylcholine, and their respective antagonists and then speculated upon physiological roles of sympathetic and parasympathetic nerves on SV during ejaculation. We found that PE and Ach both achieved good contraction of rat SV. Compared to a1b for sympathetic and M1, M2 for parasympathetic receptors, a1a and M3 are the relatively dominant subtypes on rat SV. Adrenergic and cholinergic agonists cause different trace patterns of SV contraction. We speculated that the sympathetic effect is dominant during emission to squeeze seminal fluid out and that the parasympathetic effect is dominant during ejection to provide an anti-reflux effect on the ejaculatory duct.

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Characterization of the Effects of Various Drugs Likely to Affect Smooth Muscle Tension on Isolated Human Seminal Vesicle Tissue

Cited by 18 publications

References 25 publications

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Centrally mediated ejaculatory response via sympathetic outflow in rats: role of N‐methyl‐D‐aspartic acid receptors in paraventricular nucleus

The role of sympathetic and parasympathetic nerve systems on the smooth muscle of rat seminal vesicles – experimental results and speculation for physiological implication on ejaculation

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