• Journal of The Korean Society of Clinical Toxicology
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• v.5 no.2
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• pp.123-125
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• 2007

Amitraz is a formamidine-derived insecticide and acaricide which is commonly used throughout the world. Amitraz intoxication is mediated through ${\alpha}_2$ adrenergic receptor agonist effects, similar to those of the ${\alpha}_2$ agonist clonidine. We report a case of a patient who experienced coma and hypotension after amitraz ingestion. A 37-year-old woman visited the ER with symptoms of vomiting and altered mental state. She had ingested a mouthful of liquid amitraz concentrate (12.5%), which rapidly led to vomiting, hypotension, bradycardia, hyperglycemia, and mental stupor. Supportive treatment, including mechanical ventilation and administration of inotropics, resulted in full recovery within four days.

• Journal of Dental Anesthesia and Pain Medicine
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• v.19 no.2
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• pp.83-90
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• 2019

Dexmedetomidine is a highly selective ${\alpha}2$-adrenoceptor agonist with a vast array of properties, making it suitable for sedation in numerous clinical scenarios. Its use was previously restricted to the sedation of intensive care unit patients. However, its use in pediatric dental sedation has been gaining momentum, owing to its high suitability when compared with conventional pediatric sedatives. Its properties range from sedation to anxiolysis to analgesia, due to its sympatholytic properties and minimal respiratory depression ability. Because dexmedetomidine is an efficacious and safe drug, it is gaining importance in pediatric sedation. Thus, the aim of this review is to highlight the properties of dexmedetomidine, its administration routes, its advantages over the commonly used pediatric sedatives, and especially its role as an alternative pediatric sedative.

• Biomolecules & Therapeutics
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• v.4 no.1
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• pp.103-109
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• 1996

To investigate the effect of the third intracellular loop (i3 loop) peptide of human $\beta$$_2$-adrenergic receptor on receptor agonist binding, we expressed third intracellular loop region of human $\beta$$_2$-adrenergic receptor as glutathione S-transferase fusion protein in E. coli. DNA fragment of the receptor gene which encodes amino acid 221-274 of human $\beta$$_2$-adrenergic receptor was amplified by polymerase chain reaction and subcloned into the bacterial fusion protein expression vector pGEX-CS and expressed as a form of glutathione-S-transferase (GST) fusion protein in E. coli DH5$\alpha$. The receptor fusion protein was identified by SDS-PAGE and Western blot using monoclonal anti-GST antibody. The fusion protein expressed in this study was purified to an apparent homogeneity by glutathione Sepharose CL-4B affinity chromatography. The purified i3 loop fusion proteins at a concentration of 10 $\mu\textrm{g}$/ι caused right shift of the isoproterenol competition curve of [$^3$H]Dihydroalprenolol binding to hamster lung $\beta$$_2$-adrenergic receptor indicating lowered affinity of isoproterenol to $\beta$$_2$-adrenergic receptor possibly due to the uncoupling of receptor and G protein in the presence of the fusion protein. The uncoupling of receptor and G protein suggests that i3 loop region plays a critical role on $\beta$$_2$-adrenergic receptor G protein coupling.

• Asian-Australasian Journal of Animal Sciences
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• v.10 no.5
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• pp.528-533
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• 1997

Twenty four female Sprague-Dawley rats weighing about 190 g were used to examine changes in muscle cAMP concentrations and steady-state levels of skeletal muscle ${\alpha}$-actin mRNA during chronic administration of cimaterol, a ${\beta}$-adrenergic agonist. Cimaterol was mixed in a powdered rat diet at 10 mg/kg diet. At 3 and 21 days after the start of treatment, skeletal muscle and heart samples were collected for the measurement of cAMP concentrations and skeletal muscle ${\alpha}$-actin mRNA levels. Cimaterol increased (p < 0.01) body weight gain gradually during the first seven days of the trial period, but not thereafter. Most skeletal muscle weights and the ratio of muscle weight to body weight were increased (p < 0.05) by cimaterol treatment both at 3 and 21 days. Heart weight was also increased (p < 0.05) by cimaterol treatment at 3 and 21 days, but the ratio of heart weight to body weight was increased (p < 0.05) only at 3 day. Cimaterol decreased (p < 0.05) cAMP concentration of gastrocnemius muscle at both 3 and 21 days after treatment. However, cimaterol tended (p = 0.07) to increase cAMP concentration at 3 days in the heart. Cimaterol tended (p = 0.08) to increase the steady-state level of ${\alpha}$-actin mRNA by 60% in gastrocnemius muscle at 3 days but had no effect at 21 days. The results indicate that the pattern of hypertrophic response to chronic dietary administration of cimaterol is different between cardiac and skeletal muscle. In skeletal muscles it appears that the hypertrophy induced by cimaterol is partly due to stimulated myofibrillar protein synthesis at a pre-translational level.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.43-51
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• 1989

Responsiveness of muscarinic and alpha adrenoceptor activation on endothelial cells was studied in isolated canine renal artery rings. Ach (10-100 nM), dose dependently, relaxes endothelial intact rings precontracted with phenylephrine ($IC_{50}$ of Ach was 34.5 nM). Selective mechanical destruction of the endothelium transformed the activity of this substance from vasodilatation to vasoconstriction. Acetylcholine induced relaxations could be selectively inhibited competitively by atropine, but could not be inhibited by cyclooxygenase inhibitor. Methylene blue, however, an inhibitor of soluble guanylate cyclase activity, inhibited Ach as well as sodium nitroprusside (SNP) induced relaxation. Relaxation produced by prostacyclin was not modified by methylene blue. On the other hand, alpha adrenoceptor agonist did not relax but contract canine renal artery rings possessing an intact intima precontracted with U-46619. Clonidine, however, selective alpha-2 adrenergic agonist, is more susceptible than phenylepherine, selective alpha-1 adrenergic agonist, to the inhibitory effect of contraction. These results suggest that in canine renal artery rings, 1) muscarinic receptor is responsible for releasing endothelium dependent relaxation factor (EDRF). 2) alpha-1 and alpha-2 adrenergic receptors are present in canine renal artery. 3) relaxation via EDRF is antagonized by methylene blue, providing further evidence that EDRF acts through a cGMP mechanism.

• Biomolecules & Therapeutics
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• v.11 no.2
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• pp.119-125
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• 2003

The present study was conducted to investigate the effects of bornyl acetate on arterial blood pressure and vascular contractile responses in the normotensive rats and to establish the mechanism of action. Both phenylephrine (an adrenergi$\alpha$-receptor agonist) and high potassium (a membrane-depolarizing agent) caused greatly contractile responses in the isolated aortic strips. These phenylephrine (10$^{-5}$ M)-induced contractile responses were depressed in the presence of high concentrations of bornyl acetate (10∼20 $\mu\textrm{g}$/ml), but not affected in low concentrations of bornyl acetate (2.5∼5$\mu\textrm{g}$/ml). High potassium (5.6 ${\times}$ 10$^{-2}$ M)-induced contractile responses were also greatly inhibited in the presence of bornyl acetate (2.5∼20 $\mu\textrm{g}$/ml) in a dose-dependent fashion. Bornyl acetate (1∼10 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient (data not shown). Interestingly, the infusion of a moderate dose of bornyl acetate (3mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. Collectively, these results obtained from the present study demonstrate that intravenous bornyl acetate causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic $\alpha$$_1$-receptors. bornyl acetate also causes vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic $\alpha$$_1$-receptors, in addition to the unknown mechanism of direct vasorelaxation.

• The Korean Journal of Pharmacology
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• v.20 no.2
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• pp.49-57
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• 1984

The exocrine pancreatic secretion is controlled mainly by gastrointestinal hormones as well as cholinergic nerves. The adrenergic influence on exocrine pancreas is thought not to he important and the evidences supporting this contention are still contradictory. In an effort to elucidate the adrenergic influence on the exocrine pancreas, we have determined the amylase release from pancreatic slices of rats treated with adrenergic drugs. The albino rats of either sex, weighing $60{\sim}80\;g$, were decapitated and the uncinate pancreata were isolated and incubated in screw top vials containing 2 ml krebs-Ringer bicarbonate buffer solution gassed with 95% $O_2$ and 5% $CO_2$. These vials were shaken continuously in a waterbath maintained at $37^{circ}C$, and enzyme release was stimulated with acetylcholine$(10^{-5}M)$. For chronic treatment methoxamine$(an\;{\alpha}-adrenergic\;agonist,\;5\;mg/kg)$, isoproterenol (a\;{\beta}-adrenergic\;agonist,\;10\;mg/kg) and reserpine (0.5 mg/kg) along with cholecystokinin octapeptide$(CCK-op,\;2{\mu}g/kg)$ were given i.p. in rats daily for 3, 5, 7, 9 or 12 days. For acute experiment these drugs were added directly to the incubation medium in a concentration of $10^{-5}M$ except CCK-OP $(10^{-9}M)$. The results are summarized as follows. 1) The addition of methoxamine, isoproterenol or reserpine to the incubation medium containing pancreatic slices augmented the release of amylase induced by acetylcholine and among them the effect of isoproterenol was most prominent. 2) Chronic treatment of methoxamine or reserpine caused enhancement of acetylcholine response in amylase release from pancreatic slice throughout the experimental period, but the amylase release was less than that of control by 12 days isoproterenol treatment. 3) In the pancreatic slices obtained from 12 days treatment of CCK-OP, the amylae release responding to acetylcholine was enhanced. By these finding it is suggested that methoxamine, isoproterenol and reserpine had marked influence on the exocrine pancreatic functions in rats and that these effects are due to their inherent actions rather than sympathetic nerve or adrenergic receptor function.

• The Korean Journal of Malacology
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• v.25 no.1
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• pp.15-22
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• 2009

Because it is known that bivalve hearts contain various modulatory systems activated by neuroendocrine substances, it was examined whether different classes of endogenous and synthetic drugs of neuroendocrinological importance can influence cardiac functions of the Pacific oyster Crassostrea gigas. Cholinergically active agents acetylcholine and carbachol increased heart rates while diminishing cardiac contractility. Adrenergically active substances norepinephrine (NE) and epinephrine (Epi) also induced heart rate increase and contractility decrease. An $\alpha_1$-adrenergic receptor-selective agonist phenyephrine (PE) failed to modulate either parameter. The Epi-induced heart rate increase and contractile depression were both blocked significantly by non-selective $\beta_1/\beta_2$-adrenergic antagonist propranolol. A $\beta_1$-selective antagonist atenolol prevented Epi-induced heart rate decrease but not the contractile depression, suggesting possible $\beta_2$ receptors for Epi-induced contractile depression. The three autacoids examined exerted discrete responses: histamine increased heart rate and depressed contraction; $\gamma$-amino-butyric acid increased both parameters; serotonin failed to change either parameter. The 5 piscine anesthetic agents examined, MS-222, benzocaine, quinaldine, urethane, pantocaine and pentobarbital, all failed to influence the cardiac function of oysters. Collectively, activities of neuroendocrinologically acting agents in mammals showed unexpected and distinct activities from those in mammalian cardiovascular systems. These results obtained from substances of different physiological functions can serve as a basis for understanding neuroendocrine control of the heart function in Pacific oyster.

• The Korean Journal of Pain
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• v.7 no.2
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• pp.282-286
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• 1994

The central antihypertensive agent clonidine is an ${\alpha}_2$-adrenergic agonist that possesses pain-relieving properties. It has been administered epidurally in the treatment of cancer pain and for postoperative analgesia. 1) Case 1, 62-year-old woman who suffered from neurogenic pain syndrome due to metastatic squamous cell carcinoma of spinal canal was treated. 2) Case 2, 51-year-old woman undergoing lower abdominal surgery, epidurally administered morphine did not produced postoperative analgesia. In these cases, continuous epidural administeration of clonidine (200ug/day) and 0.3% bupivacaine(12 ml/day) produce high quality pain relief. These results suggest that antinociceptive effect of epidural clonidine is assumed to result from activation of ${\alpha}_2$-adrenergic receptors in the dorsal horn of the spinal cord.

• Korean Journal of Veterinary Research
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• v.34 no.3
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• pp.493-500
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• 1994

The purpose of this study was to investigate the effects of neurotransmitters and the source of $Ca^{2+}$ in the effects of neurotransmitters on the motility of pig oviductal isthmic smooth muscle. The motility of the isolated smooth muscle was recorded by using physiological recording system. The results were summarized as follows; Acetylcholine, norepinephrine, histamine and prostaglandin $F_{2{\alpha}}(PGF_{2{\alpha}})$ caused the contraction and the contractile responses were increased in a dose-dependent manner from the concentration of $10^{-7}$ to $10^{-4}M$. The maximum contractility of acetylcholine, norepinephrine, histamine and $PGF_{2{\alpha}}$ was 65.99, 28.66, 83.99 and 47.33% of 100 mM K contraction, respectively. The contractile response induced by acetylcholine$(10^{-6}M)$ was completely blocked by the pretreatment with cholinergic receptor blocker, atropine$(10^{-6}M)$, the contractile response induced by norepinephrine$(10^{-5}M)$ was blocked by the pretreatment with ${\alpha}$-adrenergic receptor blocker, phentolamine$(10^{-6}M)$ but was not blocked and rather increased by the pretreatment with ${\beta}$-adrenergic receptor blocker. propranolol$(10^{-6}M)$, the contractile response induced by histamine$(10^{-6}M)$ was completely blocked by the pretreatment with $H_1$-histaminergic receptor blocker, pyrilamine$(10^{-6}M)$ but was increased by the pretreatment with $H_2$-histaminergic receptor blocker, cimetidine$(10^{-6}M)$. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was weakly contracted response in $Ca^{2+}$-free medium, but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was disappeared. The contractile response induced by acetylcholine$(10^{-6}M)$, norepinephrine$(10^{-5}M)$ and histamine$(10^{-6}M)$ was powerfully depressed by the pretreatment with $Ca^{2+}$-channel blocker, verapamil$(10^{-5}M)$ but the contractile response induced by $PGF_{2{\alpha}}(10^{-6}M)$ was completely inhibited.