Contraction Of Seminal Vesicle Research Articles

Low frequency neuromuscular electrical stimulation applied to the bulbospongiosus muscle prolongs the ejaculation latency in a rat model.

Premature ejaculation (PE) is common, but its true pathophysiology is not clear, and treatments are limited. We aimed to investigate the effect of neuromuscular electrical stimulation applied in different modes and frequencies to the bulbospongiosus muscle on ejaculation parameters. In this study, 24 male Wistar albino rats were used. The rats were equally divided into three groups: control, high-frequency burst (HFB) and low-frequency (LF) (n = 8 each). Neuromuscular electrical stimulation was applied to the rats for 30 min. In the HFB group, this stimulation was applied in the burst mode at 80 Hz frequency using 200 microseconds (µs) transition time. In the LF group, manual stimulation was applied using a 2 Hz frequency and 200 µs transition time. Following the intraperitoneal administration of para-chloroamphetamine at a dose of 5 mg/kg, ejaculation time, increase in basal seminal vesicle pressure, seminal vesicle maximum pressure, number and interval time of seminal vesicle contractions and bulbospongiosus muscle electromyography activities were evaluated over 30 min. There was a significant difference between the groups in terms of ejaculation time (p = 0.002). The ejaculation times of the LF, HFB and control groups were 1344.71 ± 105.9, 908 ± 62 and 672 ± 149.7 s, respectively. The post hoc analysis revealed that the ejaculation time of the LF group was significantly longer than that of the HFB and control groups (p = 0.033 and p = 0.001, respectively). The remaining parameters did not differ significantly between the groups. The results showed that low-frequency (2 Hz) electrical stimulation applied to the male rats significantly prolonged the ejaculation time. It is thus considered that applying neuromuscular electrical stimulation before planned sexual activity can prevent the rhythmic contractions necessary for completing the ejaculatory process by maintaining subtetanic continuous contraction and prolonging the ejaculation time in patients with premature ejaculation complaints.

Bilateral orchiectomy deteriorates the structure and function of seminal vesicles in a rat model.

The effects of hormone levels on ejaculation are known. In addition to thyroid hormone levels, testosterone levels are also associated with ejaculation, but no consensus has been reached on this issue. Thus, we investigated the effect of decreased testosterone levels due to bilateral orchiectomy on the chemical stimulation-induced ejaculation phases in rats. Twenty-one male Wistar rats were randomized into the orchiectomy, sham, and control groups, with seven rats in each group. Bilateral orchiectomy was performed. The ejaculation parameters were evaluated 5 days after the sham and bilateral orchiectomy operations and the waiting period in the control group. The seminal vesicle (SV) phasic contraction number and increase in basal pressure amplitude were significantly lower in the orchiectomy group (6.9 ± 3.3 and 0.6 ± 0.3 mmHg) than in the sham and control groups (11.2 ± 1.7 and 1.0 ± 0.4 mmHg, and 14.5 ± 6.6 and 1.1 ± 0.2 mmHg, respectively; p = 0.016 and p = 0.03, respectively). The interval between the SV contractions was significantly longer in the orchiectomy group (166.2 ± 104.3 s) than in the sham and control groups (76.0 ± 15.5 s and 63.1 ± 31.1 s, respectively; p = 0.014 (between groups), orchiectomy vs sham p = 0.040 and orchiectomy vs control p = 0.018). The SV weights of the rats were significantly lower in the orchiectomy group (0.14 ± 0.01 g) than in the sham and control groups (0.37 ± 0.05 g and 0.48 ± 0.03 g respectively; p < 0.0001 (between groups), orchiectomy vs sham p < 0.0001 and orchiectomy vs control p < 0.0001). The groups showed no significant differences in ejaculation time, SV basal pressure, SV maximum amplitude, and bulbospongiosus muscle contraction electromyographic activity. Our results partially clarified the relationship between decreased testosterone levels and ejaculation. Decreased testosterone levels caused statistically significant changes in SV functions and affected the ejaculation emission phase.

Central mechanisms contribute to pro-ejaculatory response induced by the combination of dopamine and 5-HT2 receptor agonist in rats

ABSTRACT Introduction Although we previously demonstrated in rats that combination of a dopamine (DA) receptor agonist and 5-HT2 receptor agonist potently and selectively facilitates the ejaculatory response through the activation of D2-like and 5-HT2C receptors, these central mechanisms are not fully understood. We therefore investigated to clarify the target level of the pro-ejaculatory effects by combination of these agonists. Methods The ejaculatory response was evaluated 30 min after drug administration by the presence of seminal materials on the paper towel as well as that adhering to the shaft of the penis. In addition, we examined isolated rat seminal vesicle contraction. Results Intrathecal administration of 5-HT2 receptor agonist m-CPP (10 μg) but not in intracerebroventricular evoked the synergistic action for ejaculation in the combination with systemic administrated DA receptor agonist apomorphine (0.1 mg/kg, s.c.). Synergy effects of combination were completely inhibited by intrathecal 5-HT2C receptor antagonist SB242084 (10 μg). Intrathecal or intracerebroventricular apomorphine (1-10 μg) evoked the pro-ejaculatory effects in the combination with systemic administrated m-CPP (0.3 mg/kg, i.p.) The selective peripherally acting D2-like receptor agonist carmoxirole did not evoked in the combination with m-CPP. Furthermore, the combination of apomorphine and m-CPP did not produce contraction of rat seminal vesicle. Conclusion These results suggest that this synergistic action for ejaculation induces in the spinal or supraspinal level but not the peripheral sites. Furthermore, the present study suggests that the activation of the spinal ejaculatory pattern generator through 5-HT2C receptors is synergistically potentiated by both spinal and supraspinal DA receptors. Disclosure Work supported by industry: no.

Comparison of the Effects of Tadalafil and α1-Adrenoceptor Antagonists on Spontaneous Seminal Emission and Electrical Field Stimulation-Induced Seminal Vesicle Contraction in Rats

BackgroundAlthough numerous reports have shown that α1-adrenoceptor (α1-AR) antagonists, which are used to treat benign prostatic hyperplasia (BPH), can cause ejaculatory disorders, few studies have investigated whether the phosphodiesterase 5 (PDE5) inhibitor tadalafil has such adverse effects. In this study, we compared the effects of tadalafil and α1-AR antagonists on seminal emission and their mechanisms of action. AimTo evaluate in normal rats the possible effects of tadalafil on spontaneous seminal emission (SSE) and seminal contraction evoked by hypogastric nerve stimulation. MethodsMale Sprague-Dawley rats were used. To assess SSE, plastic corsets were fitted around the thorax and upper abdomen of male Sprague–Dawley rats to prevent genital autogrooming. Rats were treated orally with tadalafil or an α1-AR antagonist (silodosin, naftopidil, or tamsulosin) for 3 days and housed in wire-bottomed cages. Ejaculatory plugs dropped on the bottoms of the cages were counted and weighed. To assess the intraluminal pressure of seminal vesicles, the hypogastric nerve of urethane-anesthetized rats was isolated and electrically stimulated. After stabilization of seminal vesicle contraction, the rats were intravenously administered test drugs. The expression of PDE5, endothelial nitric oxide synthetase (eNOS), and neuronal NOS (nNOS) in the seminal vesicle and vas deferens were measured by reverse-transcription polymerase chain reaction. Main Outcome MeasureThe number and weight of the ejaculatory plugs produced by corset-fitted rats and the intraluminal pressure of the seminal vesicle were evaluated. ResultsTadalafil did not affect the number or weight of the ejaculatory plugs of corset-fitted rats, whereas all α1-AR antagonists decreased both in a dose-dependent manner. The α1-AR antagonists, but not tadalafil, inhibited the seminal vesicle contraction evoked by electrical stimulation of the hypogastric nerve. The seminal vesicle and vas deferens expressed higher levels of PDE5 and eNOS mRNA and lower levels of nNOS mRNA relative to the urethra. Clinical ImplicationsTadalafil can be a treatment option in cases where there is concern about negative effects on seminal emission. Strengths and LimitationsWe demonstrated different effects of tadalafil and 3 α1-AR antagonists on rat SSE and their mechanisms of action by measuring seminal vesicle contractility in vivo. A limitation is that we used normal rats, not BPH model rats, and so our results might not apply to human BPH patients. ConclusionTadalafil did not inhibit spontaneous seminal emission or electrical field stimulation–induced seminal vesicle contraction in normal rats. The NO–cyclic guanosine monophosphate pathway is unlikely to be involved in the inhibition of seminal vesicle contraction in normal rats.Yoshinaga R, Fukui T, Yoshifuji M, et al. Comparison of the Effects of Tadalafil and α1-Adrenoceptor Antagonists on Spontaneous Seminal Emission and Electrical Field Stimulation-Induced Seminal Vesicle Contraction in Rats. J Sex Med 2019;16:680–690.

Intermedin inhibits norepinephrine-induced contraction of rat seminal vesicle

To study the effect of inter medin(IMD) on smooth muscle of rat seminal vesicles including the specific receptors and the signal pathways involved. The contraction of the seminal vesicle in response to norepinephrine (NE) and ADM2/IMD was studied by the organ bath method. The effects of antagonists for calcitonin gene related peptide (CGRP), adrenomedullin (ADM) and IMD receptors, and inhibitors of nitric oxide synthase, [L-NG-Nitroarginine Methyl Ester, L-NAME) and cAMP-dependent protein kinase (PKA), KT5720] were also investigated. The first overshoot, amplitude, frequency and basal tone were measured. There is no significant effect of IMD on the initial overshoot, frequency and the basal tone in the seminal vesicle contraction. Only the amplitude of the contraction induced by NE was inhibited by IMD. The IMD inhibitory actions on amplitude were completely blocked by hADM22-52 and L-NAME, but not by hCGRP8-37 or KT5720. Furthermore, the action was diminished by IMD17-47. The results demonstrated that the inhibitory action of IMD on NE-induced seminal vesicle contraction was mediated via the ADM receptor(s) and the nitric oxide production pathway, partially by the IMD receptor, but not by the CGRP receptor and the cAMP-PKA pathway.

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

Ejaculation 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 α1b for sympathetic and M1, M2 for parasympathetic receptors, α1a 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.

Evidence that Adrenergic and Cholinergic but Not Capsaicin-Sensitive Nerves Are Involved in the Nerve-Mediated Contraction of the Guinea Pig Seminal Vesicle

Background/Aims: The neurotransmitters participating in the nerve-mediated contraction of the guinea pig seminal vesicle (GPSV) have not been firmly established. There is debate as to the mediating role of norepinephrine and acetylcholine. Methods: We have used longitudinally and circularly oriented strips of GPSV and activated their intramural nerves by electrical field stimulation (5 and 10 Hz for 30 s). Results: Contractile responses to stimulation were enhanced by a cholinesterase inhibitor and reduced by the adrenergic α-receptor antagonist phentolamine (2.5 μmol/l). Atropine (1 μmol/l) significantly reduced responses in longitudinal preparations; a less consistent inhibition was found in circular preparations. The sensory neuron stimulant and blocker capsaicin was without effect. Conclusions: It is concluded that adrenergic nerves and also acetylcholine mediate the contractile response of the GPSV.

1021 INHIBITION OF THE FATTY ACID AMIDE HYDROLASE INCREASES LATENCY TO APOMORPHINE-INDUCED EJACULATION IN RATS

You have accessJournal of UrologySexual Function/Dysfunction/Andrology: Basic Research (II)1 Apr 20131021 INHIBITION OF THE FATTY ACID AMIDE HYDROLASE INCREASES LATENCY TO APOMORPHINE-INDUCED EJACULATION IN RATS Giovanni La Croce, Arianna Bettiga, Roberta Buono, Giorgia Colciago, Fabio Benigni, Francesco Mistretta, Francesco Montorsi, Fabio Castiglione, Maarten Albersen, and Petter Hedlund Giovanni La CroceGiovanni La Croce Milan, Italy More articles by this author , Arianna BettigaArianna Bettiga Milan, Italy More articles by this author , Roberta BuonoRoberta Buono Milan, Italy More articles by this author , Giorgia ColciagoGiorgia Colciago Milan, Italy More articles by this author , Fabio BenigniFabio Benigni Milan, Italy More articles by this author , Francesco MistrettaFrancesco Mistretta Milan, Italy More articles by this author , Francesco MontorsiFrancesco Montorsi Milan, Italy More articles by this author , Fabio CastiglioneFabio Castiglione Milan, Italy More articles by this author , Maarten AlbersenMaarten Albersen Leuven, Belgium More articles by this author , and Petter HedlundPetter Hedlund Milan, Italy More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.606AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The endocannabinoid system modulates afferent signals under certain conditions. It is not known if the endocannabinoid-regulatory enzyme fatty acid amide hydrolase (FAAH) is located to or has a function in the ejaculatory system. We aimed to examine the expression of FAAH in the seminal vesicle and vas deferens and effects of inhibition of FAAH on seminal vesicle function and ejaculation. METHODS After ethical approval, anesthetized male Sprague Dawley rats (250gram) were used for (I) recordings of intraluminal pressure of the seminal vesicle, or (II) pressures of the corpus spongiousum during apomorphine-induced (150μg/kg, s.c.) ejaculation. Effects by intraperitoneal oleoyl ethyl amide (OEtA; a FAAH inhibitor; 0.1, 1 and 10 mg/kg) or vehicle were studied. PCR, Western Blot and immunohistochemistry were used for studies of FAAH expression in rat and human tissues. Effect by OEtA (0.1-100 μM) on isolated seminal vesicle was studied in organ baths. ANOVA and T-test were used for comparisons. RESULTS PCR and WB demonstrated FAAH in rat and human seminal vesicles and vas deferens. FAAH was located in epithelial cells of both tissues. In human samples, the FAAH-2 isoform was similarly expressed. In isolated tissues, maximum inhibition by OEtA (100 μM) on nerve-induced contractions were 21±9% (human;n=5) and 22±9% (rat;n=7). In vivo, the frequencies of spontaneous seminal vesicle contractions / min. were 1.08±0.32 (baseline) and 0.58±0.13 (OEtA 10mg/kg;p<0.05), and 1.23±0.41 (baseline) and 1.45±0.52 (vehicle; ns). OEtA increased basal pressure by 34±13% (vs. 0.3±2.9% for vehicle; p<0.05). Apomorphine-induced ejaculations were registered as suprasystolic intraspongious pressure spikes with striated muscle contractions and semen-expulsion from the urethra. Latencies to the first, second and third ejaculation were 6.0±1.2, 13.1±1.9, and 19.4±2.2 min. for vehicle (n=7); 12.7±3.2 (p=0.07), 19.6±4, and 22.8±2.6 min; and 21.8±3.3 (p<0.05) for OEtA (0.1 mg/kg; n=8), 26.9±5.1 (p<0.05), and 38.7±9.5 (p<0.05) min. for OEtA (1mg/kg; n=6). No differences in the number or pressure amplitudes of ejaculations were noted for OEtA and vehicle. CONCLUSIONS FAAH is expressed in the rat and human vas deferens and seminal vesicle. FAAH inhibition seems to depress seminal vesicle excitability and prolongs latency for apomorphine-induced ejaculation in rats. Pharmacological targeting of FAAH may be an interesting principle to further develop in premature ejaculation. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e419 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Giovanni La Croce Milan, Italy More articles by this author Arianna Bettiga Milan, Italy More articles by this author Roberta Buono Milan, Italy More articles by this author Giorgia Colciago Milan, Italy More articles by this author Fabio Benigni Milan, Italy More articles by this author Francesco Mistretta Milan, Italy More articles by this author Francesco Montorsi Milan, Italy More articles by this author Fabio Castiglione Milan, Italy More articles by this author Maarten Albersen Leuven, Belgium More articles by this author Petter Hedlund Milan, Italy More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

328 Inhibition of the fatty acid amide hydrolase (FAAH) reduces in vivo spontaneous seminal vesicle contractions and increases latency to apomorphine-induced ejaculation

328 Inhibition of the fatty acid amide hydrolase (FAAH) reduces in vivo spontaneous seminal vesicle contractions and increases latency to apomorphine-induced ejaculation

In Vitro Examination of Effects of Hyperprolactinemia and Hypoprolactinemia on Seminal Vesicle Contractions

To investigate the contractile characteristics of the seminal vesicles in rats, in which hyperprolactinemia and hypoprolactinemia was induced by prolactin and bromocriptine administration. A total of 24 Wistar albino rats were randomly divided into 3 groups: control group, hyperprolactinemia group, and hypoprolactinemia group. The rats in the control group were administered 0.1 mL saline subcutaneously for 21 days. The rats in group 2 received prolactin 51 μg/kg subcutaneously for 21 days. The rats in the third group received intraperitoneal bromocriptine mesylate at a dose of 66 μg/kg. All the rats were decapitated at 21 days. The seminal vesicles were removed using a microsurgical technique, and the tissue sections were prepared (0.5 × 0.2 cm). These sections were suspended in the organ bath. Subsequently, contractions were induced using 10 μmol acetylcholine or 100 mmol potassium chloride. The amplitude values induced by potassium chloride in the prolactin group were significantly greater than those in the bromocriptine group or control group. Similarly, the amplitude values induced by acetylcholine were also significantly greater in the prolactin group than in the other 2 groups. Experimental hyperprolactinemia results in an increase in the smooth muscle contraction and tonus of the seminal vesicles. The alterations in the smooth muscle tonus in the seminal vesicles and genitourinary tract might be involved in the etiology of infertility occurring in hyperprolactinemia.

1011 EFFECT OF MELANOTAN II, A MELANOCORTIN AGONIST, ON SEXUAL BEHAVIOR SUPPRESSED BY PSYCHOLOGICAL STRESS IN MALE RATS

acetylcholine (Ach, 10 to 3 x 10M) were added with various concentrations into organ bath to induce isometric contraction of the isolated rat seminal vesicles. The dose response curve of the isolated rat seminal vesicles reacting to PE and Ach, the inhibitory dose response curve to the different adrenergic antagonists (prazosin for 1, WB-4101 for 1a, Chloroethylclonidine CEC for 1b), muscarinic antagonists (atropine for M, pirenzepine for M1, methoctramine for M2, and 4-DAMP for M3) and cross-over reaction were recorded. The twitch pattern of SVSM contraction was analyzed according to its phasic and tonic components. RESULTS: PE and Ach could both achieve good contraction of rat seminal vesicle. The IC50 of prazosin and WB-4101 were far greater than that of CEC. The IC50 of 4-DAMP was very close to atropine. PE and Ach could cause different patterns of SVSM twitch. PE induced SVSM contraction had more tonic components, but Ach induced SVSM contraction had more phasic components. CONCLUSIONS: The predominant subtypes of adrenergic and cholinergic receptors on rat seminal vesicle are £ 1a and M3 respectively. Different drugs also cause different pattern of SVSM twitch. In our speculation, sympathetic effect is more dominant during emission stage to squeeze seminal fluid out; however, parasympathetic effect is more dominant during ejection stage and provides an anti-reflux effect on ejaculatory duct. Further studies for realizing physiology of ejaculation are worthy.

Parasympathetic Influence Plays an Independent and Significant Role in Inducing the Contraction of the Seminal Vesicle of the Rat

The role of the parasympathetic pathway in seminal vesicle (SV) contraction has not been well described. The purpose of this study was to study parasympathetic effects, the dominant muscarinic receptors subtype(s), and nitric oxide (NO) effects for SV contraction. In vivo, SV pressure of mature male Wistar rats were recorded after electric stimulation (ES) of each pelvic nerve (PN; parasympathetic pathway) alone; bilateral PNs simultaneously, the L6 and S1 branches of the left PN; the left PN after ablation of sympathetic influence; the lesser splanchnic nerve (LSN) after ablation of parasympathetic influence; and the LSN after pretreatment of 4 muscarinic receptor antagonists or a NO donor-3-Morpholinosydnonimine (SIN-1). ES to the left PN caused frequency-dependent SV contraction, with similar results after ES to the right PN and bilateral PNS. ES to the L6 branch of the left PN caused significantly greater SV response than to the S1 branch. Ablation of sympathetic influence did not affect SV response to parasympathetic stimulation and vice versa. The inhibitory effects of 4-DAMP (M3 antagonist) and atropine (nonselective muscarinic antagonist) on SV response to ES were similar and significantly greater than those of pirenzepine (M1 antagonist) and methoctramine (M2 antagonist). Pretreatment of SIN-1 partially suppressed the SV response of ES to left PN. ES via the parasympathetic pathway independently induces contraction of rat SV; NO partially suppresses the SV pressure response to parasympathetic ES.

Electromyographic study of ejaculatory mechanism

Cavernosus muscle (CM), seminal vesicle (SV) and vasal ampullary (VA) contractions at ejaculation are said to be reflex mechanisms (ejaculatory reflex), which have been scarcely dealt with in the literature. We investigated the hypothesis that contraction of the CMs, SVs and VA at ejaculation is a reflex action. The electromyographic (EMG) activity of CM, SV and VA during ejaculation was recorded in 28 healthy men. The test was repeated after separate anaesthetization of the glans penis (GP), CMs, SVs, and VA in the pre-ejaculatory period. Latent ejaculatory time (LET) was calculated. CMs showed no EMG activity until rigid erection phase was reached. SVs and VA exhibited resting EMG activity which increased gradually with different stages of erection. At ejaculation, CMs, SVs and VA showed two to four intermittent contractions. The mean LET was 1.3 +/- 0.2 sec. GP anaesthetization led to the disappearance of CM, SV and VA EMG activity at ejaculation, while bland gel did not affect EMG activity. CMs, SVs and VA when anaesthetized in the pre-ejaculatory period exhibited no EMG activity at ejaculation, while saline did not affect EMG activity. Increased EMG activity of CM, SV and VA apparently denotes increase in their contractile activity. CM, SV and VA contraction on GP stimulation and ejaculation are assumed to be reflex actions and are mediated through the 'glans-cavernosovesicular reflex' (GCVR) which presumably represents the ejaculatory reflex. Changes in LET or evoked response would indicate a defect in the reflex pathway. The GCVR might act as an investigative tool in diagnosing erectile dysfunction, provided further studies are performed in this respect.

Contractile behaviour of rat seminal vesicle after gonadectomy, testosterone replacement and cyproterone treatment.

The effects of bilateral gonadectomy, testosterone replacement and cyproterone acetate treatment on seminal vesicle contractions were studied in rats in order to contribute new data on the role of androgens in the spontaneous motility of the seminal vesicle. In gonadectomized-testosterone treated rats the glands exhibited a spontaneous rhythmic activity similar to that of entire animals. The seminal vesicles of gonadectomized as well as of cyproterone treated rats also contracted spontaneously but the contractions showed a smaller amplitude. Such decrease could be related with the well-known atrophy and reduction in the number of smooth muscle cells occurring in seminal vesicles after castration. The results reported in this paper suggest that androgens are not required for the normal spontaneous activity of seminal vesicles.

Effects of Phosphodiesterase Inhibitors on the Contractile Responses of Isolated Human Seminal Vesicle Tissue to Adrenergic Stimulation

It has been suggested that the capability of the phosphodiesterase 5 (PDE5) inhibitor sildenafil citrate (VIAGRA) to retard the ejaculatory response may include modulation of the contraction of seminal vesicle (SV) smooth muscle. In fact, it has been shown that PDE inhibitors can reverse the tension of isolated human SV tissue and enhance the production of cyclic AMP and cyclic GMP. The aim of this study was to examine the effects of selective phosphodiesterase (PDE) inhibitors on both the spontaneous and electrically induced phasic contractions of isolated human SV smooth muscle. To measure the inhibition exerted by PDE inhibitors vinpocetine (PDE1-inhibitor), rolipram (PDE4-inhibitor), sildenafil, and vardenafil (PDE5-inhibitors) on the phasic contractile response of isolated SV tissue. Using the organ bath technique, the effects of increasing concentrations of the PDE inhibitors (1 nM-10 microM) were investigated on phasic contractions of SV tissue strips either mediated by means of electrical field stimulation (EFS) or the alpha(1)-adrenoceptor agonist norepinephrine. The contractile activity in response to EFS was dose-dependently reversed by the PDE inhibitors. The rank order of efficacy was: rolipram > sildenafil >or= vardenafil > vinpocetine. Mean maximum inhibition of contraction was determined as -89.6% (rolipram), -61.3% (sildenafil), -62% (vardenafil), and -46% (vinpocetine). No differences were registered with regard to the effects of sildenafil and vardenafil on the inhibition of the contraction amplitudes. The frequency of the spontaneous contractions (amplitudes/5 minutes) was reduced by 50% in the presence of 2 microM rolipram, 5 microM sildenafil or vardenafil, and 8 microM vinpocetine. Our results demonstrate that PDE inhibitors can inhibit EFS-induced and spontaneous contractile activity of isolated human SV tissue. These findings might be of importance with regard to the pharmacological treatment of premature ejaculation.

An Experimental Approach to the Interrelationship Between Hyperthyroidism and Ejaculation Latency Time in Male Rats

We investigated the effects of experimentally induced hyperthyroidism on seminal vesicle pressure measurements and bulbospongiosus muscle contractile activity in a para-chloroamphetamine (Sigma-Aldrich) induced ejaculation model in rats. Male Wistar rats were used in the study. Daily injection of 25 microg/100 gm body weight L-thyroxine (T4, Sigma-Aldrich) for 14 days was performed in 14 rats to induce hyperthyroidism. Seven L-thyroxine injected rats were in the hyperthyroid group. The remaining 7 rats (recovery group) underwent operation after a 28-day washout period to determine spontaneous recovery from hyperthyroidism. At each operation seminal vesicle catheterization was done to measure intraluminal pressure and bulbospongiosus muscle dissection was performed for electromyography. After intraperitoneal administration of 5 mg/kg para-chloroamphetamine physiological parameters related to the ejaculatory process were measured. The interval between para-chloroamphetamine administration and first ejaculation was significantly decreased in the hyperthyroid rat group compared with that in the control group (mean +/- SD 202.8 +/- 22.3 vs 465.4 +/- 104.6 seconds, p = 0.001). Seminal vesicle phasic contraction frequency was significantly higher than control group values in hyperthyroid rats (for 30 minutes 32.3 +/- 13.9, p = 0.047). The mean AUC of bulbospongiosus muscle electromyography activity was also significantly increased in this group (11.1 +/- 4.1 V per second x 10(-4), p = 0.0001). All parameters in recovery and control group rats were not significantly differed from each other. Hyperthyroidism leads to enhanced seminal vesicle contraction frequency and bulbospongiosus muscle contractile activity in rats. Hyperthyroidism affects the emission and expulsion phases of ejaculation in reversible fashion.

Muscarinic acetylcholine receptor subtypes in the rat seminal vesicle

The aim of the present study was to identify the muscarinic acetylcholine receptor (mAChR) mRNA subtypes in the rat seminal vesicle. Furthermore, the mAChR subtypes involved in the contraction of the seminal vesicle were also explored. Reverse transcriptase-polymerase chain reaction (PCR) was performed and five PCR products corresponding to M 1–M 5 mAChR mRNA subtypes were detected in this tissue. Functional pharmacological studies indicated that the rank order of mAChR antagonists in blocking the contractile effects of carbachol was p-fluoro-hexahydro-sila-difenidol ( pF-HHSiD) ≫ tropicamide > methoctramine = pirenzepine. This antagonist profile indicates that M 3 mAChR subtype is predominantly involved in the seminal vesicle contraction. Furthermore, immunohistochemical studies confirmed the presence of the M 3 mAChR subtype in the smooth muscle layers. M 2 mAChR subtype was also immunolocalized in smooth muscle cells and may be involved in the contraction of this tissue. The presence of M 2 and M 3 mAChR subtypes in the epithelial cells suggests that these receptors could be involved in the protein secretion. Taken together, the cholinergic neurotransmitter may be a factor controlling contractility and protein secretion in this tissue.

519In vitro effects of prolactin and bromocriptine on seminal vesicle contractions

519In vitro effects of prolactin and bromocriptine on seminal vesicle contractions

Expression and pharmacological characterization of α 1-adrenoceptors in rat seminal vesicle

In the present study, we investigated the α 1-adrenoceptor subtypes mediating adrenaline-induced contractions of the rat seminal vesicle by using functional studies. The reverse transcription combined with polymerase chain reaction (RT-PCR) was also used to identify of α 1-adrenoceptor mRNA subtypes. The rank order of potency of α 1-adrenoceptor antagonists in blocking the contractile effects of adrenaline was: prazosin=WB 4101⋙BMY 7378>chloroethylclonidine, indicating the presence of α 1A-adrenoceptors in the rat seminal vesicle. In the presence of nifedipine, there was a 76% reduction in the adrenaline-induced contractions. The nifedipine-insensitive component (24%) of the contractile response to adrenaline was unaffected by chloroethylclonidine. A small pool of spare α 1-adrenoceptors for adrenaline (0.10%) was also detected. All three α 1-adrenoceptor subtypes were amplified when RT-PCR was performed on total RNA isolated from rat seminal vesicle. In conclusion, these data indicate the presence of three α 1-adrenoceptor mRNA subtypes, but only α 1A-adrenoceptors are involved in the rat seminal vesicle contraction.

Orgasm after radical prostatectomy.

To evaluate the ability to obtain and the quality of orgasm after radical prostatectomy. The orgasms experienced after undergoing radical prostatectomy were evaluated in 20 men (median age 65 years, range 56-76) using a semi-structured interview and a self-administered questionnaire. In addition, the patients were asked to write a brief statement about their experiences and sensations during orgasm before and after the operation. Eighteen patients returned the questionnaire and 17 completed a statement indicating what their orgasm was like before and after radical prostatectomy. After the operation, no patient was able to maintain a completely rigid erection, but for five patients the erection was sufficient for sexual intercourse. Nine patients used a vacuum device or intracavernosal self-injection. Half the patients reported diminished sexual desire (libido) and arousal after the operation and reported the same to occur in their partners. During their "dry' orgasm post-operatively, none of the patients experienced the exquisite sensation of inevitability, the so-called "point of no return'. Seven of the 14 patients experiencing orgasm complained that their orgasmic sensation was weakened. Four patients reported normal pleasure and sensation compared to that experienced pre-operatively. Surprisingly, nine of the 14 patients had involuntary loss of urine at orgasm; for five of them this was sufficient reason to avoid any sexual contact with their partner. Radical prostatectomy may have serious consequences on libido and erectile function but sometimes other important factors, such as the absence of prostate and seminal vesicle contractions, the loss of ejaculation and involuntary loss of urine, may also compromise the orgasm.