• YAKHAK HOEJI
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• v.34 no.3
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• pp.180-191
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• 1990

A comparison was made of the effects of selective ${\alpha_1}-adrenoceptor$ agonist phenylephrine and selective ${\alpha_2}-adrenoceptor$ agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at $EC_{50}$ level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at $EC_{50}$ level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor (EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the ${\alpha_1}-adrenoceptor$ antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of ${\alpha_1}-adrenoceptor$ with dibenamine.

• Clinical and Experimental Pediatrics
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• v.50 no.6
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• pp.556-564
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• 2007

Purpose : We hypothesized that the persisting bronchial hyperresponsiveness (BHR) of adolescents with asthma remission may be controlled mainly by genetic factors, and the BHR of symptomatic asthma by airway inflammation. ${\beta}_2$-adrenoceptor gene is considered to be a candidate gene in the development of BHR. Thus, ${\beta}_2$-adrenoceptor gene polymorphism may be associated with the BHR of adolescents with asthma remission, but not with the BHR of symptomatic asthma. To evaluate this hypothesis, ${\beta}_2$-adrenoceptor gene polymorphism at 2 sites (Arg16-Gly, Gln27-Glu) were examined. Methods : Two hundred two adolescents with BHR ($PC_{20}<18\;mg/mL$) and long term remission (neither asthma-related symptoms nor medication during the previous 2 years) of their asthma (remission group), 182 adolescents with symptomatic asthma (symptomatic group), and 200 healthy adolescents (control group) were studied. Asthma phenotypes were determined using methacholine bronchial provocation test and skin prick test. Genotypes of ${\beta}_2$-adrenoceptor polymorphism were evaluated by PCR-based methods. Results : Gly/Gly allele and Gly16-Gln27 haplotype were more prevalent in the remission group than in the control group (P=0.01, P=0.02), although there was no difference between the symptomatic group and the control group. In the remission group, there was significant difference in geometric mean of $PC_{20}$ among the 3 groups subdivided by the number of Gly16-Gln27 haplotype, showing that the Gly16-Gln27 haplotype was positively associated with BHR. However, no association was found between Gly16-Gln27 haplotype and BHR in the symptomatic group. Conclusion : This study demonstrates that ${\beta}_2$-adrenoceptor polymorphism at amino acid 16 and 27 was associated with BHR persisting in adolescents with asthma remission.

• Proceedings of the Korean Nutrition Society Conference
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• 2002.11a
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• pp.86-86
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• 2002

• Biomolecules & Therapeutics
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• v.1 no.2
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• pp.151-159
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• 1993

Effect of yohimbine, a specific antagonist for presynaptic adrenoceptor, on the renal action of clonidine, a specific presynaptic adrenoceptor agonist, was investigated in dog. Clonidine, when given intravenously, produced diuretic action accompanied with augmentation of osmolar and free water clearance (Cosm and 4C_{H_2O}$), and elicited the increase of amounts of sodium and potassium excreted in urine ($E_{Na}\; and\; E_k$). These actions of clonidine were inhibited by yohimbine either injected intravenously or infused into a renal artery. Clonidine, when infused into a renal artery, produced antidiuretic action accompanied with decreased of glomerular filtration rate (GFR) and renal plasma flow (RPF), and exhibited the reduced amounts of sodium and potassium in urine. These actions of clonidine injected into a renal artery were blocked by yohimbine administered either into vein or into a renal artery. Above results suggest that yohimbine block the renal action of clonidine only in central system, do not in kidney.

• Korean Journal of Veterinary Research
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• v.33 no.3
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• pp.381-385
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• 1993

수의학 및 농업분야에서 널리 사용되고 있는 살충제인 amitraz의 효과를 척출 돼지 자궁근에서 검토하였다. Amitraz($10^{-8}{\sim}10^{-6}M$)는 발정정지기의 자궁근 수축성을 용량의존적으로 증가시켰다. Amitroaz의 이 효과는 yohimbine($10^{-8}{\sim}10^{-7}M$)에 의해 용량의존적으로 차단되었으나, prazosin($10^{-6}M$)에 의해서는 억제되지 않았다. 또한 $Ca^{2+}$-free Tyrode's solution에서나 verapamil($3{\times}10^{-5}M$)의 전처치에 의해서 amitraz의 수축효과는 완전히 억제되었다. 따라서 amitraz에 의한 발정정지기 돼지 자궁근의 수축은 ${\alpha}_2$-adrenoceptor가 중개하며 이 효과는 주로 $Ca^{2+}$ entry blocker에 감수성이 있는 $Ca^{2+}$ channel을 통한 extracellular $Ca^{2+}$ influx의 증가에 의한 것으로 여겨진다.

• Archives of Pharmacal Research
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• v.3 no.1
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• pp.23-30
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• 1980

Berberine, when administered into a ear-vein of the rabbit anesthetized with urethane, produced a long-lasting, dose related fall in blood pressure, but intraventricular berberline did not elicit the hypotensive response. This hypotensive activity of berberine was not influenced by pretreatment of vagotomization and atropine. Depressor responses induced by berberine were not impaired by diphenhydramine, chlorisondamine, guanethidine and propranolol, but reduced significantly by phentolamine pretreatment. Berberine attenuated markedly prossor responses of norepinephrine and epinephrine. These results suggest that berberine causes the hypotensive activity that is attributable to alpha adrenoceptor blockade, but not to a direct relaxant effect upon vascular smooth muscle.

• YAKHAK HOEJI
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• v.32 no.1
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• pp.55-61
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• 1988

To elucidate one of the effect of piperine on the peripheral sympathetic nervous system, influence of piperine upon the contractile action of norepinephrine, methoxamine and tyramine as well as uptake and release of $[^{3}H]-norepinephrine$ has been investigated in naive and chronic piperine-treated vas deferens of rats. $pA_2$ value for ${\alpha}_1-adrenoceptor$ of phentolamine was significantly increased. Chronic piperine-treated group was markedly shown increased efflux of $[^{3}H]-norepinephrine$ and muscular tension, but was not affected the neuronal up-take and release of $[^{3}H]-norepinephrine$. It can be concluded that potentiation of the effect of norepinephrine by acute and chronic piperine treated group may be due to the change of affinity of ${\alpha}_1-adrenoceptor$, and partly due to possible modification of storage mechanism.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.319-325
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• 2001

Several recent studies demonstrate that cAMP accumulation evokes marked changes in magnesium ($Mg^{2+}$) homeostasis. The goal of this study was to investigate the effect of melatonin, the principal hormone of the vertebral pineal gland, on $Mg^{2+}$ regulation in perfused guinea pig hearts. We hypothesized that melationin would regulate $Mg^{2+}$ efflux induced by adrenergic drugs and cAMP analogues because melatonin inhibites adneylate cyclase (AC) and phospholipase C(PLC) in the hearts. The $Mg^{2+}$ content in the perfusate was significantly higher in the presence than in the absence of melatonin. The addition of forskolin, isoproterenol or dimaprit to perfused hearts induced a marked $Mg^{2+}$ efflux. These effluxes were not inhibited by melatonin. The $Mg^{2+}$ efflux could also be induced by phenylephrine, a ${\alpha}_1$-adrenoceptor agonist. This phenylephrine-induced $Mg^{2+}$ efflux was inhibited by melatonin. In addition, the phenylephrine-induced $Mg^{2+}$ efflux was potentiated by PMA, a protein kinase C(PKC) activator. This $Mg^{2+}$ efflux was inhibited by melatonin. In conclusion, these data suggest that melatonin regulates $Mg^{2+}$ homeostasis and the inhibitory effect of melatonin on ${\alpha}_1$-adrenoceptor-stimulated $Mg^{2+}$ efflux may occur through an inhibition of PLC pathway in perfused guinea pig hearts.

• Korean Journal of Veterinary Research
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• v.41 no.4
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• pp.497-503
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• 2001

Evidence from the last 10 years have been suggested that melatonin mainly produce a depressant effect on the cardiac system, but we found an activating effect of melatonin on heart rate in this research. To determine the hypothesis that melatonin has dual effects on physiological behaviour of cardiac system, we investigated the effects of melatonin on heart rate in isolated rat atria and anesthetized rats. Regardless of concentration, melatonin produced bradycardia in the 84 cases of 148 experiments (57 %) and tachycardia in the 64 cases of 148 experiments (43 %). And in atrium, melatonin produced a decrease automaticity in 52 cases of 86 experiments (60 %) and increase automaticity in 40 % (34/86 cases). Also, these effects are not significnat relationship with concetration of melatonin. The melatonin-induced bradycardia in vivo was inhibited by pretreatment of atropine or bilateral cervical vagotomy. Also, in isolated atrium the melatonin-induced decrease in automaticity was inhibited by pretreatment of atropine. These melatonin-induced responses were potenitated by pretreatment of propranolol. The melatonin-induced tachycardia in vivo was inhibited by pretreatment of propranolol, nifedipine or bilateral cervical vagotomy, but not by pretreatment of atropine. The melatonin-induced incease in automaticity in isolated atrium was converted to decrease in automaticity by pretreatment of propranolol. In addition, the change in heart rate caused by adrenoceptor agonists was inhibited by pretreatment of melatonin. These results indicate that melatonin-induced bradycardia may be related to a muscarinic receptor activation and melatonin-induced tachycardia may be related to a $\beta$-adrenoceptor stimulation.

• Journal of Chest Surgery
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• v.24 no.7
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• pp.637-646
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• 1991

Effect of noradrenaline and endothelium on the high K+ or Ach-induced contraction were investigated in the pig myocardial coronary artery. The helical strip of isolated pig myocardial coronary artery was immersed in the Tris-buffered Tyrode`s solution equilibrated with 100% O2 at 37oC and its isometric tension was measured. High K+ and Ach-induced contraction were dose-dependent. By denuding the endothelium, dose-contraction curve of K+ was not shifted significantly to the left and upward, but that of Ach was shifted significantly to same direction 25 mM K+ - and Ach-induced contraction were relaxed by norepinephrine[NE]. NE-induced relaxation was blocked by the pretreatment of propranolol, which was known as b-adrenoceptor blocker. And, phenylephrine known as a-adrenoceptor agonist, and clonidine known as a-adrenoceptor agonist increased the 25mM K+ - induced contraction respectively. Denuding of endothelium did not show any significant effects on NE-induced relaxation and contraction increased by phenylephrine and clonidine. Tyramine increased 25mM K+ - induced contraction further. The contractile response by tyramine on the 25mM K+ - induced contraction was not blocked by the pretreatment of phentolamine, but was partially blocked by the pretreatment of atropine. From the above results, it is suggested that activation of a1-and a2-adrenoceptors induce the contraction, activation of b-adrenoceptors induce the relaxation, and NE-induced relaxation is mainly due to activation of b-adrenoceptors. Also it is suggested that denudation of endothelium did not influence NE-induced relaxation, but influence Ach-induced contraction in the pig myocardial coronary artery.