Recent reports suggest that the responses of the detrusor muscle to the hypogastric nerve stimulation and some autonomic drugs may not be identical among various species. In this study, the responses of the isolated detrusor muscle strips of the Amyda Japonica and the rabbit to catecholamines were compared, and the type of the adrenergic-receptors was investigated. The results obtained were as follows : 1. Catecholamines (norepinephrine and epinephrine) evoked only contraction in the isolated detrusor muscle of the Amyda Japonica and relaxation in the preparation of the rabbit. 2. The contraction-response in the Amyda Japonica was blocked in the presence of regitine, an adrenergic alpha-receptor blocking agent. 3. The relaxation-response in the rabbit was abolished by pre-treatment with propranolol, an adrenergic beta-receptor blocking agent. 4. Acetylcholine elicited contraction in both of the isolated detrusor muscle strips of the Amyda japonica and the rabbit, and the response was completely blocked in the presence of atropine. 5. The results described above suggest that catecholamines exert excitatory effect on the detrusor muscle of the Amyda japonica as it contains adrenergic alpha-receptors and inhibitory effect on the same preparation of the rabbit as it contains the adrenergic beta-receptors. Key Word : amyda japonica,alpha receptor, beta receptor.
Acetylcholine ; Atropine ; Autonomic Agents* ; Catecholamines ; Phentolamine ; Propranolol ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, beta ; Relaxation

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

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

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

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

PURPOSE: To investigate the role of beta-adrenergic receptors, and the relevance of NO-mediated & calcium channel-mediated signal transduction in seminal vesicle contractions. MATERIALS AND METHODS: Rabbit seminal vesicle strip preparations were applied to an organ bath system under standard condition. Smooth muscle contractions were induced by alpha and/or beta-adrenergic agonists (norepinephrine, phenylephrine, isoproterenol), and blocked by alpha (prazosin) and/or beta (propranolol)-blocker, an NO donor (sodium nitroprusside) and calcium channel blocker (verapamil). The contractility of the smooth muscle was measured by EC50. RESULTS: Norepinephrine, phenylephrine and isoproterenol produced a sudden increase in the contractions of the smooth muscle. The order of the adrenergic agonists in relation to increases in the contractility was norepinephrine>phenylephrine>isoproterenol. The contractions induced by norepinephrine and phenylephrine were partially blocked by prazosin, and those by isoproterenol were completely blocked by propranolol. The contraction induced by norepinephrine was partially blocked by sodium nitroprusside and verapamil, in dose dependant manners. CONCLUSIONS: Seminal vesicle contractions are mediated mostly by alpha-adrenergic receptors, and seem to be partly mediated by beta-adrenergic receptors. The contractility of seminal vesicle seems to be partly regulated by the NO-cGMP-cascade and calcium channel mediated signal transduction.
Adrenergic Agonists ; Adrenergic beta-Agonists ; Baths ; Calcium ; Calcium Channels ; Humans ; Isoproterenol ; Muscle, Smooth ; Nitroprusside ; Norepinephrine ; Phenylephrine ; Prazosin ; Propranolol ; Receptors, Adrenergic ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, beta ; Seminal Vesicles* ; Signal Transduction ; Tissue Donors ; Verapamil

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*

PURPOSE: The lacrimal sac and nasolacrimal duct are surrounded by a wide cavernous system of veins and arteries, and the blood vessels of the cavernous body are innnervated by the autonomic nervous system. The purpose of this study was to determine the effect of an adrenergic agonist on the lumen width of the nasolacrimal drainage system. METHODS: Dacryocystography was performed on 35 patients with only epiphora and not nasolacrimal duct obstruction. The anteroposterior (AP) diameters and the oblque diameters of the nasolacrimal ducts were measured. Next, 18 patients were infused with 0.5 ml Alphagan-P(R) (alpha-2 adrenergic receptor agonist), 17 patients were infused with 0.5 ml DL methylephedrine hydrochloride (alpha-1 and alpha-2 adrenergic receptor agonist), and dacryocystography was performed again to determine the change in the lumen width of the nasolacrimal drainage system. RESULTS: The alpha-adrenergics caused a significant increase in the lumen width of the nasolacrimal drainage system, and the changes were more pronounced in the nasolacrimal duct than in the lacrimal sac. Although the nasolacrimal duct widening was more notable in the Alphagan-P(R) infusion group than the DL methylephedrine hydrochloride infusion group, there was no significant statistical difference. Patients' subjective symptoms improved in both groups. CONCLUSIONS: The alpha-adrenergics constrict the blood vessels of the cavernous body, leading to the increase in the lumen width of the nasolacrimal drainage system. This effect was more significant in the Alphagan-P(R) infusion group. In conclusion, infusion of alpha-adrenergics in patients with functional nasolacrimal duct obstruction can be considered as an alternative to surgical management.
Adrenergic Agonists ; Arteries ; Autonomic Nervous System ; Blood Vessels ; Caves ; Drainage ; Ephedrine ; Humans ; Lacrimal Apparatus Diseases ; Nasolacrimal Duct ; Receptors, Adrenergic ; Receptors, Adrenergic, alpha-2 ; Veins

Risperidone is an atypical antipsychotic medication commonly used to treat psychotic illness, such as schizophrenia. It has strong serotonin and dopamine receptor antagonism and antagonist activity at alpha-adrenergic receptors and histamine receptors. An overdose of risperidone can cause tachycardia, hypertension, hypotension, prolonged QT interval, and bradycardia. Risperidone overdose is rare,but life-threatening. Here, we present the rare case of a 33- year-old woman who ingested risperidone overdose for the purposes of suicide, developing hemodynamically unstable bradycardia with trifascicular block, leading to fatality. Lessons from our case report are of urgent consideration for temporary pacemaker insertion, and use of alpha-1 agonist, such as phenylephrine in cases of hemodynamically unstable bradycardia by risperidone overdose. Prompt and appropriate identification and interventions are essential for the successful management of risperidone overdose.
Bradycardia ; Female ; Humans ; Hypertension ; Hypotension ; Phenylephrine ; Receptors, Adrenergic, alpha ; Receptors, Dopamine ; Receptors, Histamine ; Risperidone ; Schizophrenia ; Serotonin ; Suicide ; Tachycardia

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