• The Journal of the Korean dental association
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• v.10 no.9
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• pp.575-583
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• 1972

• Journal of dental hygiene science
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• v.2 no.1
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• pp.47-51
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• 2002

The concentration of intracellular $Ca^{2+}$ was measured by spectrofluorometer after rat submandibular acinar cells were loaded with fura-2/AM(fura-2). After isoproterenol and octanol were administered while letting submandibular gland acinar cell placed in a perfusion chamber flow through a standard solution, the changes of $Ca^{2+}$ concentration were measured. When they were administered separately, there showed little changes of intracellular $Ca^{2+}$ concentration. When they were administered at the same time, however the concentration of intracellar $Ca^{2+}$ was shown to increase. When forskolin, an adenylate cyclase activater, was administerd together with octanol the response looked similar to the response of isoproterenol. In case of the extracellular $Ca^{2+}$ was removed by omitting $Ca^{2+}$ in standard solution and treating EGTA, isoproterenol and forskolin does not affect to the concentration of intracellular $Ca^{2+}$. Therefore, it was certified that the increase of intracellular $Ca^{2+}$ was caused from outside the cell. In order to know that the $Ca^{2+}$ influx is related with capacitative entry pathway, godolinium, blocker of that pathway was treated. With the result of that experiment there was no complete control of the increase in the concentration of intracellular $Ca^{2+}$. However, speed and amount of $Ca^{2+}$ increase was comparatively diminished.

• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.245-252
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• 1993

Amiloride is a potassium sparing duretic which specifically inhibits $Na{^+}$ channels. In the present study, we investigated the possible interaction of amiloride with $A_1$ adenosine receptors-adenylyl cyclase system in crude adipocytic plasma membrane fractions prepared from Sprague-Dawley rats. When the function of $G_i$ protein (inhibitory guanine nucleotide binding protein) was assessed by determining the effects of GTP on isoproterenol-stimulated adenylyl cyclase activity, the inhibitory effect of high concentrations of GTP was not observed in the presence of amiloride. In contrast, the adenosine receptor-mediated inhibition of the enzyme activity, as determined empolying 2-chloroadenosine, was either unchanged or even more enhanced by amiloride depending on the concentrations of 2-chloroadenosine. Thus, it appears that GTP- and receptor-mediated inhibitory function of $G_{i}$ proteins can be separated from one another. Receptor-mediated function of $G_{s}$ protein did not appear to be significantly affected by amiloride, since the inhibition of isoproterenol-stimulated adenylyl cyclase activity by propranolol under the same conditions was not significantly altered by amiloride. The enhancement of 2-chloroadenosine-mediated inhibition of adenylyl cyclase by amiloride was maintained in the presence of 150 mM NaCl. In summary, these results suggest that amiloride interacts both with $A_{l}$ adenosine receptors and with $G_i$ proteins in adipocytic membranes. Its binding to the $A_1$ adenosine receptors appears to facilitate the coupling of the receptors with $G_i$ proteins thereby enhancing the inhibition of isoproterenol-stimulated adenylyl cyclase activity by $A_1$ adenosine agonist, and the direct interaction with $G_i$ proteins appears to remove the GTP-dependent inhibitory effect on adenylyl cyclase activity.

• The Korean Journal of Physiology
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• v.14 no.1
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• pp.25-30
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• 1980

It has been well known that beta-adrenoceptor is responsible for the renin release stimulatory and alpha-adrenoceptor may be inhibitory. It has been observed accidently that alpha-adrenergic agonist can inhibit renin release by just changing the medium temperature in Vitro experiment in this laboratory. A series of experiments were performed to clarify this interesting phenomena in Vitro experiment. Rat renal slices were incubated in PSS medium under gas phase at $37^{\circ}C$. The following results were observed. 1) Isoproterenol and norepinephrine resulted in renin release stimulatory in dose-dependent by the concentrations of $10^{-9}$ to $10^{-5}\;M/L$ at $37^{\circ}C$. 2) Norepinephrine resulted in renin release inhibitory in dose dependent by the concentrations of $10^{-7}$ to $10^{-5}\;M/L$, and almost no effect by isoproterenol $10^{-6}\;M/L$ at $20^{\circ}C$. 3) Phenoxybenzamine pretreatment at $37^{\circ}C$ accentuated isoproterenol stimulatory effect at $37^{\circ}C$. 4) Phenoxybenzamine pretreatment at $20^{\circ}C$ attenuated isoproterenol stimulatory effect at $37^{\circ}C$. These data suggest that the renal adrenoceptor(s) related to renin release maybe a single entity, and can be interconverted different forms in certain conditions.

• The Korean Journal of Pharmacology
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• v.8 no.1
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• pp.41-47
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• 1972

The author studied the adrenotropic receptors of isolated vas deferens from Ditrema temmincki Bleeker, using adrenergic activators such as epinephrine, norepinephrine, isoproterenol and phenylephrine, and adrenergic blocking agents such as phenoxybenzamine and propranolol. The results are as follows: 1. The vas deferens was stimulated by epinephrine, norepinephrine and phenylephrine, but not affected by isoproterenol. 2. The excitatory effect of phenylephrine on the vas deferens was completely blocked by phenoxybenzamine, but more stimulated by propranolol. 3. The excitatory effects of epinephrine and norepinephrine were markedly reduced by phenoxybenzamine, but stimulated by propranolol. 4. The vas deferens pretreated with phenoxybenzamine and propranolol was not affected by epinephrine and norepinephrine. 5. The vas deferens was not affected by isoproterenol and also not affected by the pretreatment with either kind of blocking agent plus isoproterenol. 6. It seemed that the vas deferens had both alpha-excitatory receptor and beta-receptor, but it was difficult to detect the character of beta-receptor whether it was inhibitory or excitatory.

• Advances in Traditional Medicine
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• v.10 no.4
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• pp.278-287
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• 2010

The present study was undertaken to evaluate the protective effect of ethanol (EtAS), ethyl acetate (EAAS) and aqueous (AQAS) extracts of Argyreia speciosa (AS) roots against Isoproterenol (ISO)-induced myocardial infarction in rats. The animals were exposed to isoproterenol (200 mg/kg. s.c) twice at an interval of 24 hrs. Cardioprotective effect was assessed by observing ECG parameters, serum marker enzymes and histopathology of the heart. Pretreatment of EAAS, and EtAS (200 mg/kg) resulted in a significant (P < 0.001) increase in P wave, QRS complex and R-R interval, whereas heart rate, QT interval and cardiac cycle were maintained near to normal values. EtAS and EAAS showed significant (P < 0.05; P < 0.001) reduction in all the tested diagnostic markers compared to ISO treated group. Histological studies on the structural changes of heart tissue supported the protective activity of AS. The result suggest that treatment of AS prior to ISO has a significant role in protecting the animals from ISO induced myocardial infarction.

• Korean Journal of Biological Psychiatry
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• v.3 no.1
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• pp.46-50
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• 1996

This study was designed to examine the basal cyclic AMP levels and the $10^{-5}mol/L$ isoproterenol-stimulated cyclic AMP levels of lymphocytes, by which ${\beta}$-adrenoceptor function was shown, between to normal controls and 17 drug free patients(8 major depresive patients and 9 dysthymic patients), who were diagnosed by DSM-III-R. The severity of depression was assessed by Hamilton Rating Scale for Depression (HDRS). Cyclic AMP levels were measured by radioimmunoassay(double antibody). The results were as follows ; 1) HDRS score was significantly higher in major depressive patients($41.8{\pm}4.6$) than in dysthymic patients($24.0{\pm}4.2$)(p<005). 2) There was no Significant difference in basal cyclic AMP levels among normal controls($3.9{\pm}1.7pmol/10^6cells/10min$), major depressive patients($2.1{\pm}0.5pmol/10^6cells/10min$), and dysthymic patients($3.9{\pm}1.8pmol/10^6cells/10min$). 3) There was significant difference in net cyclic AMP levels($10^{-5}mol/L$ isoproterenol-stimulated cyclic AMP levels minus basal cyclic AMP levels) among normal controls($16.5{\pm}6.0pmol/10^6cells/10min$), major depressive patients($3.0{\pm}1.4pmol/10^6cells/10min$), dysthymic patients($10.9{\pm}4.4pmol/10^6cells/10min$)(p <005). 4) The net cyclic AMP levels were significantly correlated with HDRS scores in major depressive patients(${\gamma}=-0.8^6$, p<0.05), but not in dysthymic patients(${\gamma}=0.43$, p=0.25). In conclusion, we suggested that the dysthymic disorder might differ from the molar depressive disorder not only in the severity of depressive symptoms but also in ${\beta}$-adrenergic responsiveness of lymphocytes, which was regarded as a biological marker of depressive disorder.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.86-86
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• 1993

혈관근의 수축 또는 이완 반응에서 $Na^{＋}$/Ca$^{2＋}$ exchange계의 역할을 알아보고자 먼저 가토와 흰쥐 흉부 대동맥에서 수축과 이완 반응을 검색하고 이때의 혈관 이완 반응을 증개하는 cAMP와 cGMP농도를 측정하였다. 내피세포가 존재한 표본에서 acetylcholine은 norepinephrine 수축 반응을 이완시켰고 이완 반응은 methylene blue로 소실되었으며 isoproterenol과 nitroprusside는 내피 존재와 제거 양표본에서 이완 반응을 일으켰으며 이때 isoproterenol은 CAMP농도를, nitroprusside는 cGMP농도를 증가시켰다.

• The Korean Journal of Pharmacology
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• v.5 no.1
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• pp.35-38
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• 1969

1.On isolated atrial preparation of frog, effects of sympathomimetic amines were investigated. 2. Isoproterenol, epinephrine, norepinephrine, and phenylephrine produced positive chronotropic and inotropic effects. The relative potencies for the effects of these agents were: isoproterenol > epinephrine> norepinephrine> phenylephrine. Methoxamine had no effects or depressed the atria. 3. Pronethalol antagonized the positive effects of these adrenergic agents competitively. 4. Regitine did not affect the effects of these agents. 5. These data indicate that the adrenergic agents activate the atrial tissue of the frog via stimulation of adrenergic beta-receptor.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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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.