alpha1-adrenoceptor antagonists are first-line agents for the treatment of lower urinary tract symptoms suggestive of benign prostatic hyperplasia, while their adverse effects on sexual function are reported frequently in recent years, especially the induction of ejaculatory dysfunction. This review presents the distribution of alpha 1-adrenoceptors in the male genital system and the relationship of alpha1-adrenoceptors with ejaculatory function. It also highlights the interesting phenomenon of ejaculatory dysfunction related to these drugs and its possible mechanism, with the intention to provide some essential clues for further research on this problem as well as some references to safer use of these drugs in clinical settings.
Adrenergic alpha-1 Receptor Antagonists ; Adrenergic alpha-Antagonists ; adverse effects ; pharmacology ; Ejaculation ; physiology ; Erectile Dysfunction ; chemically induced ; physiopathology ; Humans ; Male ; Receptors, Adrenergic, alpha-1 ; physiology

Benign prostatic hyperplasia (BPH) is a common senile disease, and its main clinical manifestation is lower urinary tract symptom (LUTS), which has long been afflicting old male patients. Previous study showed that alpha1-receptor in the prostate was involved in the development of LUTS. At present, alpha1-receptor blocker is generally accepted as a choice drug for treating BPH and relieving LUTS. The article reviews the tissue distribution of alpha1-receptor and clinical application of alpha1-receptor blocker.
Adrenergic alpha-1 Receptor Antagonists ; Adrenergic alpha-Antagonists ; adverse effects ; pharmacokinetics ; therapeutic use ; Humans ; Male ; Prostatic Hyperplasia ; drug therapy ; Receptors, Adrenergic, alpha-1 ; analysis

PURPOSE: To evaluate the efficacy of an alpha-1 adrenergic receptor (α1-AR) blocker for the treatment of female voiding dysfunction (FVD) through a pressure-flow study. METHODS: This was a randomized, double-blind, placebo-controlled trial. Women aged ≥18 years with voiding symptoms, as defined by an American Urological Association symptom score (AUA-SS) ≥15 and a maximum flow rate (Qmax) < 15 mL/sec with a voided volume of >100 mL and/or a postvoid residual (PVR) volume >150 mL, were randomly allocated to either the alfuzosin or placebo group. After 8 weeks of treatment, changes in the AUA-SS, Bristol female lower urinary tract symptoms (BFLUTS) questionnaire, Qmax/PVR, and voiding diary were compared between groups. Patients’ satisfaction with the treatment was compared. Patients were categorized into 3 groups according to the Blaivas-Groutz bladder outlet obstruction (BOO) nomogram: none, mild, and moderate to severe. Subgroup comparisons were also made. RESULTS: Of a total of 187 women, 154 (79 alfuzosin, 75 placebo) were included in the analysis. After 8 weeks of treatment, the AUA-SS decreased by 7.0 in the alfuzosin group and by 8.0 in the placebo group. Changes in AUA-SS subscores, BFLUTS (except the I-sum), the voiding diary, and Qmax/PVR were not significantly different between groups. Approximately 54% of the alfuzosin group and 62% of the placebo group were satisfied with the treatment. No significant difference was observed between groups according to the presence or grade of BOO. CONCLUSIONS: Alfuzosin might not be more effective than placebo for treating FVD. The presence or the grade of BOO did not affect the results. A further study with sufficient power is needed to determine the efficacy of α1-AR blockers for the treatment of FVD.
Adrenergic alpha-Antagonists ; Female ; Humans ; Lower Urinary Tract Symptoms ; Nomograms ; Receptors, Adrenergic, alpha-1 ; Urinary Bladder Neck Obstruction ; Urodynamics

PURPOSE: The aim of this study was to assess the potential involvement of a specific subtype of 5-hydroxytryptamine (5-HT), 5HT(2) receptors in neurally-induced contractions of the human detrusor. METHODS: Contractile responses to electrical field stimulation (EFS) were examined in human isolated urinary bladder muscle strips. The potentiation of EFS-induced detrusor contraction was examined by adding cumulative concentrations of a 5-HT and 5-HT(2) receptor agonist, α-methyl-serotonin (α-Me-5-HT) (1nM–100μM) in the presence or absence of a 5-HT₂ antagonist, ketanserin (5-HT(2A)>5-HT(2C)) or naftopidil (5-HT(2B)>5-HT(2A)) (0.3–3μM). RESULTS: 5-HT and α-Me-5-HT potentiated EFS-induced contraction with a maximal effect (E(max)) of 37.6% and 38.6%, respectively, and with pEC(50) (negative logarithm of the concentration required for a half-maximal response to an agonist) values of 8.3 and 6.8, respectively. Neither ketanserin nor naftopidil at any concentration produced a rightward displacement of the α-Me-5-HT concentration response curve. Instead, the E(max) of α-Me-5-HT increased in the presence of ketanserin at 0.3–1μM and in the presence of naftopidil at 1μM to 51% and 56%, respectively, while the E(max) in the presence of vehicle alone was 36%. The highest concentration (3μM) of either drug, however, fully reversed the enhancement. CONCLUSIONS: The potentiating effect of α-Me-5-HT on neurally-induced contraction of human urinary bladder muscle strips was not found to be mediated via any 5-HT(2) receptor subtypes. The underlying mechanism for the enhancement of the α-Me-5-HT potentiating effect on detrusor contractility by ketanserin and naftopidil remains unknown; however, our results suggest that these drugs may be useful for treating contractile dysfunction of the detrusor, as manifested in conditions such as underactive bladder.
Humans* ; Ketanserin* ; Prostatism ; Receptors, Adrenergic, alpha-1 ; Receptors, Serotonin ; Serotonin ; Urinary Bladder Neck Obstruction ; Urinary Bladder*

BACKGROUND: The effect of spinal adrenergic and cholinergic receptors on the anti-nociceptive effect of intrathecal ginsenosides was determined in a rat postoperative pain model. METHODS: Catheters were placed into the intrathecal space of male Sprague-Dawley rats. Postoperative pain was evoked by an incision to the plantar surface of a hind paw. Withdrawal thresholds was used as a nociceptive parameter and was measured with a von Frey filament. After observing the effect of intrathecal ginsenosides, an alpha-1 adrenergic receptor antagonist (prazosin), an alpha-2 adrenergic receptor antagonist (yohimbine), a muscarinic acetylcholine receptor antagonist (atropine), and a nicotinic acetylcholine receptor antagonist (mecamylamine) were given 10 min before administration of the ginsenosides to analyze the contribution of spinal adrenergic and cholinergic receptors on the antinociceptive effect of ginsenosides. RESULTS: Paw incision decreased withdrawal threshold in incised site of paw, but no change of withdrawal threshold was not seen in non-incised site. The intrathecal ginsenosides increased withdrawal threshold of the incised paw in a dose-dependent manner. Pre-treatment with both prazosin and intrathecal yohimbine antagonized the anti-nociceptive effect of the ginsenosides. However, pre-treatments with atropine or mecamylamine had any effect on the antinociceptive activity of ginsenosides. CONCLUSIONS: Intrathecal ginsenosides are effective in attenuation of postoperative pain induced in the rat model. Anti-nociceptive action of ginsenosides is partially mediated by spinal adrenergic receptors, but does not appear to be related to spinal cholinergic receptors.
Animals ; Atropine ; Catheters ; Ginsenosides ; Humans ; Male ; Mecamylamine ; Pain, Postoperative ; Prazosin ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic ; Receptors, Adrenergic, alpha-1 ; Receptors, Adrenergic, alpha-2 ; Receptors, Cholinergic ; Receptors, Muscarinic ; Receptors, Nicotinic ; Spinal Cord ; Yohimbine

Prazosin blocks the alpha-1 adrenergic receptor of sympathetic nerve. The effects of prazosin in patient with epidural lumbar anesthesia were analyzed with blind test. In a prospective randomized study, we compared a group of 25 patients who received prazosin with a control group of 58 patients. Forty-one( 70.7 %) of 58 patients developed acute urinary retention. In 11 of 25 patients(44 %), who were medicated with prazosin(3mg. per 18 hours) urinary retention was noted ( p >0.05). Mean catheterization rate in urinary retented patients was 1.61 in control group(41 cases), and was 1.27 in prazosin medicated group( 11 case) (p <0.05). Prazosin is an effective drug not only to prevent acute urinary retention but also to reduce the need for catherization.
Anesthesia ; Anesthesia, Epidural* ; Catheterization ; Catheters ; Humans ; Prazosin* ; Prospective Studies ; Receptors, Adrenergic, alpha-1 ; Urinary Retention*

OBJECTIVETo observe the association between ADRA1A gene polymorphism and autoantibodies against the alpha1-adrenergic receptor in hypertensive patients.

METHODSA total of 396 patients with essential hypertension admitted to our hospital were selected and autoantibodies in sera were detected by ELISA, and patients were divided into the autoantibody positive and negative group. Genomic DNA was extracted from erythrocytes obtained from EDTA-treated blood by the Blood DNA extraction kit. Gene polymorphisms were detected by ligase detection reaction (LDR), including rs574584, rs1048101, rs3739216 and rs3802241. The frequency of genotypes and haplotype were analyzed.

RESULTSThe frequencies of detected genotypes between the autoantibody against the alpha1-adrenergic receptor positive group and negative group were similar (P > 0.05) while significant difference was in the frequencies of haplotypes (all P < 0.05). The frequencies of genotypes with rs1048101 (genotype C/C, C/T, P = 0.017) and rs3802241 (genotype A/A, A/G, P = 0.004) were significant different in autoantibody positive group compared to negative group in patients with stage 2.

CONCLUSIONADRA1A gene polymorphism might correlate with the alpha1-adrenergic receptor autoantibody production in hypertensive patients.

Autoantibodies ; blood ; Genotype ; Haplotypes ; Humans ; Polymorphism, Genetic ; Receptors, Adrenergic, alpha-1

PURPOSE: To assess the effectiveness of alpha-1 adrenergic receptor blockers (α1-blockers) in the treatment of female lower urinary tract symptoms (LUTS). METHODS: A literature search was conducted using the PubMed/MEDLINE, Embase, and Cochrane Library databases. Fourteen studies with 1,319 patients were ultimately included. The study comprised 2 analyses: a comparison of urinary symptom scores, maximal flow rate (Qmax), and postvoid residual (PVR) urine volume before and after α1-blocker administration in 8 prospective, open-label studies and 5 randomized clinical trials (RCTs); and an evaluation of the same variables in α1-blocker and placebo groups in 4 RCTs.
Female ; Humans ; Lower Urinary Tract Symptoms ; Prospective Studies ; Receptors, Adrenergic, alpha-1

OBJECTIVETo determine whether autoantibodies against the cardiac G-protein-coupled beta 2- and alpha 1-adrenergic and AT1 receptors are related to patients with primary hypertension.

METHODSSynthetic peptides corresponding to amino acid sequences of the second extracellular loops of the beta 2- and alpha 1-adrenergic and AT1 receptors were respectively used as antigens to screen sera from patients with hypertensive heart diseases (n = 50) as well as simple hypertension (n = 40) and healthy blood donors (n = 40) using ELISA test.

RESULTSThe positive ratio of autoantibodies against beta 2 and alpha 1 and AT1 receptors in patients with hypertensive heart diseases were significantly higher than patients with simple hypertension and healthy donors. The geometric mean titers of autoantibodies against beta 2- and alpha 1-adrenergic and AT1 receptors had no difference between the patients with hypertensive heart diseases and the patients with simple hypertension, but the geometric mean titers of two groups were higher than healthy donors. In the patients with hypertensive heart diseases, 81.0% of the patients with autoantibodies against beta 2-adrenergic receptor had autoantibodies against alpha 1-adrenergic receptor and 76.2% had autoantibodies against AT1 receptors. The percent of the autoantibodies against three receptors in patients with hypertensive heart diseases were 52.4%.

CONCLUSIONSAutoantibodies against beta 2- and alpha 1-adrenergic and AT1 receptors play an important role in the pathophysiological changes of primary hypertension, and may participate myocardial and vessel remodeling.

Adult ; Aged ; Autoantibodies ; blood ; Female ; Humans ; Hypertension ; immunology ; Male ; Middle Aged ; Receptor, Angiotensin, Type 1 ; immunology ; Receptors, Adrenergic, alpha-1 ; immunology ; Receptors, Adrenergic, beta-2 ; immunology

PURPOSE: Whereas many studies have focused on the vesical changes of the alpha1 adrenergic receptor (AR) subtypes in partial outlet obstruction, few studies have addressed the modulation of the alpha1 AR subtypes after spinal cord injury (SCI). Therefore, we studied the modulation of the alpha1 ARs in urinary bladder in a rat SCI model. METHODS: Four weeks after a SCI, the whole vesical bodies from eight female Sprague-Dawley rats and from eight controls were harvested. The total RNA was extracted from the samples and was used to prepare cDNA. We developed standard plasmid constructs of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and three alpha1 ARs (alpha1a, alpha1b, and alpha1d) to convert the cycle threshold (Ct) values from real-time polymerase chain reaction (RT-PCR) into subtype mRNA concentrations. The detected Ct values of 16 samples from RT-PCR were interpolated into the standard plasmid curves. RESULTS: All serially diluted standard samples showed very good linearity. The mRNA expression of GAPDH was higher in the SCI group, whereas the mRNA expression of all alpha1 ARs was lower in the SCI group than in the control animals. The alpha1a, alpha1b, and alpha1d mRNA expression in the controls was 81.7%, 3.3%, and 15.1%, respectively, whereas the alpha1a, alpha1b, and alpha1d mRNA expression in the SCI group was 33.5%, 5.2%, and 60.9%, respectively. CONCLUSIONS: SCI moderates the alpha1 AR mRNA subtypes in the urinary bladder. The relatively increased alpha1d or decreased alpha1a AR mRNA expression may be a therapeutic candidate for controlling the symptoms of neurogenic bladder after SCI.
Animals ; DNA, Complementary ; Female ; Humans ; Oxidoreductases ; Plasmids ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptors, Adrenergic ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, alpha-1 ; RNA ; RNA, Messenger ; Spinal Cord ; Spinal Cord Injuries ; Urinary Bladder ; Urinary Bladder, Neurogenic