PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12861842

[Medication for premature ejaculation].

Wei-Fu Wang·De-Xin Dong·Song Cen
View original source ↗Export metadata ↓

Abstract

Drugs for the treatment of premature ejaculation (PE) are divided to two categories: oral drugs and local drugs. Oral drugs include antidepressive drugs, alpha-adrenoceptor blocking drugs, phosphodiesterase type V blocking drugs and Chinese herbal medicine. Local drugs include local surface drugs, intracavernosal injective drugs and local urethra drugs. Antidepressive drugs are extensively used, which have moderate efficacy, relatively more side effects and high recurrence rate; alpha-adrenoceptor blocking drugs are seldom used and are less effective than antidepressive drugs; phosphodiesterase type V blocking drugs like sildenafil have good efficacy and few side-effects and are worthy to be studied further. Local surface drugs like SS-Cream have good efficacy and few side-effects and are worthy to be applied and promoted; local urethral drugs like MUSE and Befar may become a new method to treat PE after being further studied. Medication for premature ejaculation shall be made specific and suitable as much as for each individual patient.

Explore related subjects

Adrenergic alpha-AntagonistsAntidepressive AgentsDrugs, Chinese HerbalEjaculationHumansMalePhosphodiesterase InhibitorsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Wei-Fu Wang, De-Xin Dong, Song Cen. 2003. [Medication for premature ejaculation].. https://pubmed.ncbi.nlm.nih.gov/12861842/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Androgen-induced norepinephrine release mediating guinea pig seminal vesicle smooth muscle proliferation: potential role of pre-synaptic alpha2-adrenoceptors.

BACKGROUND: Recent studies from our laboratory have demonstrated that androgen-induced basal norepinephrine (NE) release is responsible for the onset of proliferation in seminal vesicle smooth muscle (SVM) cells during early puberty. With subsequent sexual maturation, SVM was irreversibly differentiated to an androgen-resistant-amitotic state in which basal NE release remained elevated and resistant to androgen withdrawal or repletion. Based on these findings, we hypothesized that this irreversible elevation of basal NE release during pubertal development is caused, at least in part, by the down-regulation of pre-synaptic NE feedback inhibition, secondary to irreversible reduction in the expression of neuronal (pre-synaptic) alpha(2)-adrenoceptors. Functional alpha(2)-adrenoceptors are selectively localized to pre-synaptic sites in SVM. METHODS: To test this hypothesis, we employed ligand binding techniques with [(3)H]RX821002, an antagonist which labeled all alpha(2)-adrenoceptor sub-types. Initial experiments focused on analysis of competitor specificity to identify the predominant alpha(2)-adrenoceptor sub-type in SVM. Subsequently, we quantified the changes in the receptor concentration (B(max)) for [(3)H]RX821002 at the point of maximal dihydrotestosterone (DHT)-induced change in basal NE release. RESULTS: Based on competitor specificity for [(3)H]RX821002, the alpha(2D)-adrenoceptor sub-type predominated in SVM. We treated pre-pubertal castrate animals with DHT for 7 days, which was previously demonstrated to maximally induce basal NE release. This treatment reduced the pre-synaptic alpha(2)-adrenoceptor B(max) 4-fold. In animals which had been castrated as adults, the B(max) for [(3)H]RX821002 remained irreversibly suppressed. CONCLUSIONS: The DHT-dependent reduction in the alpha(2)-adrenoceptor concentration is consistent with the developmental pattern of increased basal NE release. These findings support the hypothesis that the down-regulation of pre-synaptic NE feedback is mechanistically involved in the irreversible elevation of basal NE release. NE mediates proliferation in SVM in early pubertal development. Thus, the androgen-dependent pubertal growth of smooth muscle cells may be indirectly controlled at the level of neurotransmission.

Adrenergic alpha-Antagonists↗
PubMed2003

Interaction between the noradrenergic and serotonergic systems in locomotor hyperactivity and striatal expression of Fos induced by amphetamine in rats.

It is classically considered that Amphetamine acts by increasing extracellular dopamine levels. However, some data suggest a relevant role of other neurochemical systems. The striatum is of particular interest to the study of this question. We have investigated the involvement of the noradrenergic and serotonergic systems and their possible interaction in the striatal responses to Amphetamine using a double behavioral and immunohistochemical approach (i.e., changes in locomotor activity and striatal expression of Fos). In normal rats, Amphetamine induced locomotor hyperactivity and striatal expression of Fos. Pretreatment with the alpha1-adrenergic-receptor antagonist Prazosin or lesion of the serotonergic system significantly reduced the locomotor hyperactivity and striatal Fos expression induced by Amphetamine. Administration of Prazosin to rats with serotonergic denervation did not produce any further reduction in the Amphetamine-induced locomotor hyperactivity or striatal Fos expression compared with that observed in rats with serotonergic denervation only. Amphetamine did not induce a detectable increase in Fos expression in dopamine-denervated striata, and elicited intense rotation towards the dopamine-denervated side. This suggests that striatal dopamine release is essential in the Amphetamine-induced effects on striatal neurons. However, the noradrenergic system plays an important role, and the serotonergic system is necessary for mediating the effects of the Amphetamine-induced noradrenergic stimulation. Concurrent stimulation of dopaminergic and serotonergic receptors appears necessary to regulate Amphetamine-induced responses in the striatal neurons.

Adrenergic alpha-Antagonists↗
PubMed2003

Arterial baroreflex control of muscle blood flow at the onset of voluntary locomotion in mice.

To assess the role of arterial baroreflex control in muscle blood flow (MBF) and voluntary locomotion, mean arterial pressure (MAP), MBF, and electromyograms (EMGs) were measured in freely moving mice before (CNT) and after blocking the afferent or efferent pathway of arterial baroreflexes, carotid sinus denervation (CSD), or intraperitoneal administration of phentolamine (BLK), respectively. MAP was measured through a catheter placed in the femoral artery. MBF was measured with a needle-type laser-Doppler flowmeter and recorded through a low-pass filter with an edge frequency of 0.1 Hz. The frequency and duration of locomotion were judged from EMG recordings in the hindlimb. These probes were implanted at least 2 days before the measurements. Muscle vascular conductance (MVC = MBF/MAP) in all groups started to rise within 1 s after the onset of locomotion, but the increasing rate in CSD and BLK was significantly higher than in CNT for the first 9 s (P < 0.001). MAP in CSD and BLK significantly decreased below the baseline within 1 s and this was highly correlated with the increase in MVC for the first 9 s (R2 = 0.842, P < 0.001), whereas MAP in CNT increased significantly 8 s after the onset of locomotion. Although the total period of movement in a free-moving state for 60 min was not significantly different between CNT and CSD (P > 0.1), the frequency of movement with a short duration of 0.1-0.4 min was higher in CSD than in CNT (P < 0.001), which was highly correlated with the reduction in MAP accompanying each period of movement (R2 = 0.883, P < 0.01). These results suggest that arterial baroreflexes suppress vasodilatation in contracting muscle to maintain MAP at the onset of voluntary locomotion, and are necessary to continue a given duration of locomotion in mice.

Adrenergic alpha-Antagonists↗