• 대한약리학회지
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• 제22권1호
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• pp.24-33
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• 1986

본 연구에서는 개구리(Rana nigromaculata)의 피부에 있어서 전위차(PD), 단락전류(SCC) 및 total skin conductance(TSC)에 미치는 제종 adrenergic agonist 및 그 차단제의 영향을 관찰하여 개구리 피부에 adrenoceptors의 존재를 확인하고 Na 수송에 있어 그들의 역할을 구명코자 하였다. 1.Norepinephrine(NE, $6{\times}10^{-8}-6{\times}10^{-5}M$), phenylephrine($PE,5{\times}10^{-6}-5{\times}10^{-4}M$)의 PD 및 epinephrine(Epi, $5.5{\times}10^{-7}-5.5{\times}10^{-5}M$)의 PD 및 SCC 증가효과는 약물의 투여농도에 비례하였으며, Epi의 최대효과는 NE나 PE의 것보다 약하였다. 2. 이러한 PD 및 SCC의 증가효과는 alpha 1 adrenoceptor 차단체인 prazosin $2{\times}10^{-6}M$에 의해서 억제되었으며, 특히 Epi의 증가효과는 불가역성 alpha receptor 차단제인 phenoxybenzamine $3.3{\times}10^{-5}M$에 의하여 완전히 차단되며 대량의 Epi에 의해서는 PD 및 SCC의 감소를 초래하였다. 3. Beta adrenoceptor agonist인 isoproterenol$(5{\times}10^{-7}-5{\times}10^{-6}M)$에 의해 농도증가에 비례한 PD 및 SCC의 감소가 일어났으며, 이는 선택적 bete receptor 차단제인 propranolol $4{\times}10^{-6}M$에 의해 차단되었다. 또한 Epi의 PD 및 SCC 증가효과는 propranolol $4{\times}10M$에 의하여 강화됨을 볼 수 있었다. 4. Alpha 2 adrenoceptor agonist인 clonidine 및 guanabenz도 PD 및 SCC의 증가를 가져왔으며 이러한 효과는 alpha 2 receptor 차단제인 yohimbine에서 보다 Alpha 1 receptor 차단제인 prazosin에 의해 더 잘 억제되었다. 이상 실험의 결과 개구리 복부피부에도 포유동물에서와 같이 adrenergic alpha 및 beta receptor가 존재하며 alpha receptor는 PD 및 SCC의 증가를, beta receptor는 PD 및 SCC의 감소를 매개하여, 개구리 피부의 Na 수송에 있어 adrenergic system이 중요한 조절작용을 하고 있음을 알 수 있었다. 그러나 여기에 관여하는 alpha receptor는 다른 포유류에서와 같이 alpha 1 및 alpha 2 adrenoceptor로 구분할 수는 없었다.

• Archives of Pharmacal Research
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• 제9권4호
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• pp.219-222
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• 1986

Dose-dependent increasesin blood glucose were produced by epinephrine and clonidine in fasted male mice. Isoproterenol was ineffective in increasing blood glucose at lower doses ($10^{-8}M$/kg-$10^{-7}M$/kg); with higher dose ($10^{-6}M$/kg) the glucose level was increased. The hyperglycemia induced by epinephrine was inhibited by yobimbine, prazosin and propranolol, indicating that the hyperglycemic effect of epinephrine is mediated by alpha-1, alpha-2 and beta adrenoceptor. When clonidine (10$^{-6}$ M/kg) was administered simultaneously with sioproterenol ($10^{-6}M$/kg), an enhenced hyperglycemic effect was observed. The increment produced by clonidine plus isoproterenol was higher than that by clonidine alone. These increment produced by clonidine plus isoproterenol was higher than that by clonidine alone. These results suggest that stimulation of alpha-2 adrenoceptor may be reponsible for the exertion of the hyperglycemic effect by beta agonists in fasted mice.

• The Korean Journal of Pain
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• 제9권2호
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• pp.318-325
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• 1996

Background: Sympathectomy relieves pain in sympathectically maintained pain, and subcutaneous injection of norepinephrine(NE) can rekindle mechanical allodynia. However, the mechanism of rekindling is not clear. The purpose of this study is to investigate which subtype of $\alpha$-adrenoceptor is involved in NE-induced rekindling of mechanical allodynia in sympathectomized neuropathic rats. Methods: Neuropathic injury was produced by tightly ligating the left L5 and L6 spinal nerves of 36 male Sprague-Dawley rats and bilateral lumbar sympathectomy was done at two weeks postoperatively. Starting at 7 days after sympathectomy, rekindling of mechanical allodynia was induced by NE and clonidine injected into the left paw, which was reversed by pretreatment of phentolamine and idazoxan. Mechanical allocynia was quantified by measuring the frequency of foot lifts to two von Frey filaments applied to the paw. Results: All tested rats displayed well-developed signs of mechanical allodynia at the left paw that were abolished by a bilateral lumbar sympathectomy. Subcutaneous (s.c.) injection of NE (0.05 ${\mu}g$) into the affected paw of sympathectomized neuropathic rats rekindled previous mechanical allodynia. These effects could be mimicked by an ${\alpha}_2$-receptor agonist clonidine, but not by an ${\alpha}_1$-receptor agonist phenylephrine. The NE-induced rekindling of mechanical allodynia was significantly reduced by prior s.c. injection of a mixed $\alpha$-receptor antagonist phentolamine (20${\mu}g$) and ${\alpha}_2$-receptor antagonist idazoxan(20${\mu}g$), but not by a ${\alpha}_1$-receptor antagonist terazosin (20${\mu}g$). The pretreatment of idazoxan produced dose-related inhibition of NE-induced rekindling of mechanical allodynia. The rekindling induced by ${\alpha}_2$-receptor agonist clonidine (5${\mu}g$) was also reversed by prior s.c. injection of ${\alpha}_2$-receptor antagonist idazoxan (20${\mu}g$). Conclusion: Subcutaneous injection of NE into the paw of sympathectomized neuropathic rats rekindles mechanical allodynia, which is reversed by an ${\alpha}_2$-, but not by an ${\alpha}_1$-receptor antagonist. Therefore, rekindling of mechanical allodynia in sympathectomized neuropathic rats is mediated by ${\alpha}_2$-adrenoceptor.

• Asian-Australasian Journal of Animal Sciences
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• 제7권3호
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• pp.397-400
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• 1994

The effect of xylazine administration on plasma cortisol, prolactin, glucose and packed cell volume (PCV) responses to immobilization and heat stress was investigated. Immobilization of rats for 2 hours by ligation of the fore and hind legs strongly caused approximately two-fold increase in plasma cortisol and prolactin levels. Plasma glucose and PCV were not significantly changed. Pretreatment of immobilized rats with xylazine (20 mg/kg body weight i.m.) resulted in approximately 20% reduction in both plasma cortisol and prolactin concentrations. A marked hyperglycemia and increase in the PCV value was observed. On the other hand, rats exposed to acute heat stress ($40^{\circ}C$, and 60% relative humidity) for 2 hours, also developed two fold increase in both plasma cortisol and prolactin concentrations and the pretreatment with xylazine caused a 20% reduction in the levels of both hormones. Plasma glucose level was not significantly changed in heat stressed rats but it was markedly increased after pretreatment with xylazine. PCV was significantly incrcased under heat stress and pretreatment with xylazine induced a pronounced elevation in this value. It was suggested that stimulation of cortisol and prolactin secretion in response to immobilization or heat stress can be partially reduced by an alpha 2-adrenergic agonist.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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• pp.753-761
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• 1998

Preconditioning of a heart with small doses of catecholamines induces a tolerance against the subsequent lethal ischemia. The present study was performed to find a specific receptor pathway involved with the catecholamine preconditioning and to test if adenosine plays a role in this cardioprotective effect. Isolated rat hearts, pretreated with small doses of ${\alpha}-\;or\;{\beta}-adrenergic$ agonists/antagonists, were subjected to 20 minutes ischemia and 20 minutes reperfusion by Langendorff perfusion method. Cardiac mechanical functions, lactate dehydrogenase and adenosine release from the hearts were measured before and after the drug treatments and ischemia. In another series of experiments, adenosine $A_1\;or\;A_2$ receptor blockers were treated prior to administration of adrenergic agonists. Pretreatments of a ${\beta}-agonist,\;isoproterenol(10^{-9}{\sim}10^{-7}\;M)$ markedly improved the post-ischemic mechanical function and reduced the lactate dehydrogenase release. Similar cardioprotective effect was observed with an ?-agonist, phenylephrine pretreatment, but much higher $concentration(10^{-4}\;M)$ was needed to achieve the same degree of cardioprotection. The cardioprotective effects of isoproterenol and phenylephrine pretreatments were blocked by a ${\beta}_1-adrenergic$ receptor antagonist, atenolol, but not by an ${\alpha}_1-antagonist,$ prazosin. Adenosine release from the heart was increased by isoproterenol, and the increase was also blocked by atenolol, but not by prazosin. A selective $A_1-adenosine$ receptor antagonist, 1,3-dipropyl-8-cyclopentyl xanthine (DPCPX) blocked the cardioprotection by isoproterenol pretreatment. These results suggest that catecholamine pretreatment protects rat myocardium against ischemia and reperfusion injury by mediation of ${\beta}_1-adrenergic$ receptor pathway, and that adenosine is involved in this cardioprotective effect.

• 생물정신의학
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• 제7권1호
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• pp.80-84
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• 2000

Clozapine의 부작용 중 타액의 과잉분비의 원인을 알아보기 위하여 순천향대학교 천안병원 신경정신과에 입원한 환자 중 정신분열병 환자 21명(남자 12명, 여자 9명)을 대상으로 시행한 본 연구결과는 다음과 같다. 1) 정신분열병 환자에게 clozapine을 투여한 후 타액의 분비는 유의하게 증가하였다. 2) Clozapine을 투여한 후 타액의 과잉분비를 보인 정신분열병 환자에게 clonidine을 투여한 후 타액의 분비는 유의하게 감소하였다. 3) Clozapine에 의한 타액의 과잉분비는 ${\alpha}$-아드레날린성 작용에 의한다는 것을 강하게 시사한다.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1997년도 학술발표회
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• pp.27-27
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• 1997

The effects of $a_1$-adrenoceptor stimulation on intracellular $Ca^{2+}$ ([C $a^{2+}$]$_{i}$ ) transient, contraction, and L-type $Ca^{2＋}$ current ( $I_{Ca,L}$) were studied in single cells isolated from ventricles of guinea pig hearts. Phenylephrine, $\alpha$$_1$-adrenergic agonist, (5$\times$10$^{-5}$ ~10$^{-4}$ M) produced a biphasic pattern of inotropism： transient negative response (decrease in contraction by 23.9$\pm$2.5% of control) followed by a sustained positive response (increase in contraction by 60.0$\pm$3.4%, mean $\pm$ SD, n=12).(omitted)ted)

• Journal of Dental Anesthesia and Pain Medicine
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• 제19권2호
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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.

• 대한임상독성학회지
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• 제5권2호
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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.

• Biomolecules & Therapeutics
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• 제4권1호
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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.