This study was designed to determine the effect of electrical field stimulation (EFS) and adrenergic agonist on the contractility of vasectomized prostatic and epididymal segments at postvasectomized 2, 5 and 10 weeks, and to observe innervation changes of the vas deferens after vasectomy. The contractile response was recorded on a polygraph via force transducer and expressed as the g tension per 100 mg tissue. And we reviewed histopathologic sections stained with S-100 protein by light microscopy. The results were as follows: 1. In control groups, contractile responses of prostatic and epididymal segments to EFS (4, 8, 16, 32 &64 Hz) were gradually increased by increasing frequencies. But contractile responses of vasectomized epididymal segments to all frequencies of EFS declined. Contractile responses of vasectomized prostatic segments were significantly greater than that of vasectomized epididymal segments (p<0.05). 2. Contractile responses of epididymal segments to phenylephrine hydrochloride 0.00001M were significantly greater than that of prostatic segments (p<0.05). Contractile responses of prostatic segments were tend to decline. In epididymal segments, contractile response of post-vasectomized 5 weeks group was significantly greater than that of control and post-vasectomized 2 weeks groups (p<0.05). 3. In control and vasectomized prostatic segment, nerve bundles were strongly positive and intact histopathologically for the S-100 protein immunohistochemical stain. In epididymal segment, nerve bundles were intact in control group. However, vacuolar degeneration tend to be gradually increased and stained weakly by increasing duration in vasectomized epididymal segment. These results suggest that the progression of degenerative change of adrenergic innervation after vasectomy may play an important role in progressively decreasing contractility of the vas deferens after vasectomy.
Adrenergic Agonists ; Adrenergic alpha-Agonists* ; Animals ; Microscopy ; Phenylephrine ; Rats* ; S100 Proteins ; Transducers ; Vas Deferens* ; Vasectomy*

BACKGROUND: Recent studies have documented increased release of endothelin(ET) during acute attack of asthma. The purpose of this study is to observe the link between plasma level and urinary excretion of each and changes during acute exacerbation. METHOD: Plasma and 24 hour urine were collected from sixteen asthmatics during acute exacerbation, twice ; first day of symptomatic exacerbation and two weeks after treatment. Controls were ten healthy normal subjects. All patients were treated with corticosteroid and beta-2 adrenergic agonist on admission. ET was determined by radioimmmunoassay and had 100% cross reactivity with ET-1, 67% with ET-2, 84% with ET-3, and 8% with Big-ET. RESULTS: Plasma ETs were significantly elevated during acute attack of asthma compared with those in remission and controls. However, there was no significant changes in urine ET concentrations or total ET amounts in 24 hour urine during exacerbation upto two weeks. Those levels of urine ET in asthmatics were still higher than controls. ET concentrations in plasma or urine were not correlated with pulmonary functional parameters and hypoxemia. CONCLUSION: The findings suggests that increased plasma ETs are related with exaggerated release during acute asthma. Urinary ET excretion is increased in asthma. However, urine ET changes during exacerbation should be observed in a larger and longer scale.
Adrenergic Agonists ; Anoxia ; Asthma* ; Endothelin-2 ; Endothelins* ; Humans ; Plasma*

PURPOSE: To investigate the effects of tetrahydrozoline (THZ) on the survival of cultured human trabecular meshwork cells (HTMC) and the permeability of HTMC monolayer. METHODS: Primary cultured HTMC were exposed to an adrenergic agonist (0.01, 0.1, 1.0 or 10 µM THZ) for 1 day and 3 days. Carboxyfluorescein permeability through the HTMC monolayer was measured using Transwell. Cellular viability and nitric oxide (NO) production were assessed using MTT and Griess assays, respectively. RESULTS: THZ did not affect the cellular survival (p > 0.05) or NO production (p > 0.05). THZ significantly increased the carboxyfluorescein permeability through the HTMC monolayer in a dose-dependent manner compared with non-exposed control (p < 0.05) after exposure for 1 and 3 days. CONCLUSIONS: THZ does not affect the survival of HTMC but decreases the permeability of HTMC monolayer in a dose-dependent manner. Thus, THZ may possibly decrease trabecular outflow.
Adrenergic Agonists ; Humans ; Nitric Oxide ; Permeability* ; Trabecular Meshwork*

In order to examine the properties of catecholic receptor-mediated activation of Na-K-ATPase reaction, author have studied. 1) the structure-activity relationships of various catechol analogues as stimulants of rat cortical Na-K-ATPase. 2) the stereospecificity of alpha and beta-adrenergic agonists on their activation of enzyme system and 3) the relationship of the receptive sites to the enzyme Na-K-ATPase and the effect of EDTA. The observed results were as follows: 1) Noradrenalin, dopamine and isoproterenol stimulated the Na-K-ATPase activity in rat cortical nomogenate. 2) The Na-K-ATPase activation elicited by catecholamines could not be antagonized by beta-receptor blocker, phentolamine and alpha-receptor blocker, propranolol decreased the increase in activity evoked by catecholamine, but it could not inhibit completely. 3) alpha-receptor blocker, phenoxybenzamine inhibited the noradrenalin activation on Na-K-ATPase, and decreased the effect of EDTA on the Na-K-ATPase activity.
Adrenergic Agonists ; Adrenergic beta-Agonists ; Animals ; Brain* ; Catecholamines ; Dopamine ; Edetic Acid ; Isoproterenol ; Phenoxybenzamine ; Phentolamine ; Propranolol ; Rats ; Structure-Activity Relationship

Adrenergic receptors are members of the G-protein coupled receptor superfamily. Recent studies revealed that these adrenergic receptors are playing an important role in the growth and metastasis of prostate cancer cells. The expression of adrenergic receptors rises significantly in prostate cancer cells and tissues. Agonists of these receptors promote the growth and mobility of prostate cancer cells, while antagonists may suppress their proliferation, trigger their apoptosis, and inhibit their metastasis. Clinically, receptor antagonists can significantly reduce the risk of prostate cancer and improve its prognosis after androgen depravation therapy. This article presents an overview on the roles of adrenergic receptors in prostate cancer.
Adrenergic Agonists ; pharmacology ; Adrenergic Antagonists ; pharmacology ; Apoptosis ; Humans ; Male ; Prostatic Neoplasms ; metabolism ; pathology ; Receptors, Adrenergic ; drug effects ; physiology

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

A large number of β-adrenergic receptor (β-AR) agonists and antagonists are widely used in the treatment of cardiovascular diseases and other diseases. Nonetheless, it remains unclear whether these commonly used β-AR drugs can activate downstream β- arrestin-biased signaling pathways. The objective of this study was to investigate β-arrestin2 recruitment effects of β-AR agonists and antagonists that were commonly used in clinical practice. We used TANGO (transcriptional activation following arrestin translocation) assay to detect the β-arrestin2 recruitment by β-AR ligands in HEK293 cell line (HTLA cells) stably transfected with tetracycline transactivator protein (tTA) dependent luciferase reporter and β-arrestin2-TEV fusion gene. Upon activation of β-AR by a β-AR ligand, β-arrestin2 was recruited to the C terminus of the receptor, followed by cleavage of the G protein-coupled receptors (GPCRs) fusion protein at the TEV protease-cleavage site. The cleavage resulted in the release of tTA, which, after being transported to the nucleus, activated transcription of the luciferase reporter gene. The results showed that β-AR non-selective agonists epinephrine, noradrenaline and isoprenaline all promoted β-arrestin2 recruitment at β1-AR and β2-AR. β1-AR selective agonists dobutamine and denopamine both promoted β-arrestin2 recruitment at β1-AR. β2-AR selective agonists procaterol and salbutamol promoted β-arrestin2 recruitment at β2-AR. β-AR non-selective antagonists alprenolol and pindolol promoted β-arrestin2 recruitment at β1-AR. β1-AR selective antagonists celiprolol and bevantolol showed β-arrestin2 recruitment at β1-AR. β2-AR selective antagonists butoxamine showed β-arrestin2 recruitment at β1-AR. These results provide some clues for the potential action of β-AR drugs, and lay a foundation for the screening of β-arrestin-biased β-AR ligands.
Humans ; beta-Arrestin 2/metabolism* ; HEK293 Cells ; Adrenergic beta-Agonists/pharmacology* ; Isoproterenol/pharmacology* ; Receptors, Adrenergic, beta-2/metabolism* ; Norepinephrine/pharmacology*

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

BACKGROUND: Ropivacaine is an amino amide local anesthetic that has an advantage of a low-toxicity profile. Clonidine, an alpha2 adrenergic agonist, is known to prolong and intensify anesthesia from epidural local anesthetics. The aim of this study was to evaluate the dose-response effects of added clonidine to ropivacaine-fentanyl epidural anesthesia for lower extremity surgery. METHODS: Forty-five patients undergoing lower extremity surgery were randomly allocated to three groups to be given the following agents by an epidural route: 0.75% ropivacaine 15 ml+fentanyl 50microgram with clonidine 50microgram (group I), 100microgram (group II), or 150microgram (group III). Onset and maximal height of sensory block, and duration of sensory and motor block were assessed. Also, blood pressure, heart rate and sedation score were measured. RESULTS: Duration of sensory and motor block of groups II and III was significantly longer than that of group I, but there was no difference between group II and group III. Two segment regression times were significantly different among the three groups. Onset of sensory block, blood pressure, heart rate, and sedation scores were not significantly different among the three groups. CONCLUSIONS: The addition of Clonidine 100 and 150microgram prolonged duration of anesthesia more than 50microgram with ropivacaine-fentanyl epidural anesthesia for lower extremity surgery.
Adrenergic Agonists ; Anesthesia ; Anesthesia, Epidural* ; Anesthetics, Local ; Blood Pressure ; Clonidine* ; Heart Rate ; Humans ; Lower Extremity*

To evaluate the effect of Morphine during spinal anesthesia with alpha-adrenergic agonist, we used 0.18 mg of epinephrine, 90 ug of clonidine and 0.3 mg of morphine with 12 mg of T-cain respectively and compared hemodynamic and analgesic effects of each drug. Eighty patients were divided into four groups as follows; Group I (n=20); T-cain with clonidine, Group II (n=20); T-cain with epinephrine, Group III (n=20); T-cain with clonidine and morphine, and Group IV (n=20); T-cain with epinephrine and morphine. The results were as follows; 1) The onset time of analgesia and the time reached to the highest level of sensory loss were most rapid in the epinephrine and morphine group. 2) The duration of analgesia was significantly prolonged in the group of epinephrine and morphine than the group of epinephrine and clonidine. 3) It was more likely complicated in the morphine groups than others but there was no significance. 4) Although the heart rate was gradually decreased over 60 min. after anesthesia, there was no significance between the groups. 5) Systolic and diastolic blood pressure were decreased mainly over 30~45 min. after anesthesia, but there was no significance. In conclusion, epinephrine can be sustituted for clonidine because analgesic duration was not significantly changed, and the duration of analgesia was prolonged by morphine.
Adrenergic alpha-Agonists ; Analgesia ; Anesthesia ; Anesthesia, Spinal* ; Blood Pressure ; Clonidine* ; Epinephrine* ; Heart Rate ; Hemodynamics ; Humans ; Morphine*