• 동의생리병리학회지
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• 제22권5호
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• pp.1223-1235
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• 2008

This experiment was performed to investigate the effects of Hyeonsamdansameum(HDE) on hypertension. For the study of HDE, we had divided Sprague-Dawley rats to three groups-normal, control, HDE. The control group was injected subcutaneous with monocrotaline(50 mg/kg). The treatment group was injected subcutaneous with monocrotaline(50 mg/kg) and orally administered with HDE extract for 4 weeks(once a day, 208 mg/kg). Then we measured blood pressure, heart rate, on the plasma aldosterone, catecholamine, electrolyte, uric acid, BUN, creatinine, and observed the lung, cardiac muscle. liver. etc. The results of these were as follows: 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity and superoxide dismutase(SOD) - like activity were increased. reactive oxygen species (ROS) was decreased. Angiotensin converting enzyme(ACE) inhibitory activity was increased in a concentration-dependent by HDE. HDE significantly increased body weight in monocrotaline hypertensive rat, so supported nearly normal group. HDE significantly decreased blood pressure and heart rate in monocrotaline hypertensive rat. HOE significantly decreased aldosterone in adrenocortical hormones. HDE significantly decreased dopamine. norepinephrine, epinephrine. Na+. Cl- were intended to decrease. K+ was decreased significantly by HDE. Uric acid. BUN were significantly decreased and creatinine was intended to decrease by HDE. HDE inhibited lung, liver and heart injury connected with hypertension. These results suggest that HDE is usefully applied in treatment and prevention of hypertension.

• 동의생리병리학회지
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• 제20권6호
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• pp.1485-1496
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• 2006

Various kinds of related parameters on hypertension such as anti-oxygen effect, ACE, weight of body, hwart and kidney, blood pressure, heartbeat rates, contents of aldosterone, catecholamine, change rates, of plasma constituents, uric acid, BUN, creatinine were determined to verify the effects on hypertension by Kamisamul-tang (KSMT). And the results are concluded as follows. KSMT did not show any cytotoxicity at the range of concentration (1-250 ${\mu}g/m{\ell}$) on the human fibroblast cell (hFCs). KSMT decreased the production of reactive oxygen species (ROS) and DPPH generation depending on the concentration. KSMT significantly inhibited angiotensin converting enzyme(ACE) activity depending on the concentration compared with control. KSMT maintained body weight of body, heat and kidney nearly normal group in hypertensive rat induced by DOCA-salt. KSMT significantly blood pressure and heart beat rate compared with control in hypertensive rat induced by DOCA-salt. KSMT significantly decreased aldosterone, dopamine, norepineph- rine, epinephrine compared with control in hypertensive rat induced by DOCA-salt. KSMT significantly decreased the level of potassium and cloride compared with control wheareas increased that of calcium significantly in hypertensive rat induced by DOCA-salt. KSMT significantly decreased the level of uric acid and BUN compared with control in hypertensive rat induced by DOCA-salt. It is verified experimentally tat Kamisamultang(KMST) which has been used broadly as a clinical therapeutics in oriental medicine is effective for anti-hypertension mechanism. And it could be applied to develope the reliable prescriptions for anti-hypertension in the future.

• 대한약리학회지
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• 제26권2호
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• pp.177-183
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• 1990

간-부분절제후 재생과정에서 간 polyamine 대사에 교감신경계가 촉진적으로 간여하는지를 확인하기 위하여 본 실험을 시행하였다. Guanethidine 25mg/kg를 1회 (G-1), 또는 매일 1회씩 3(G-3), 5(G-5) 및 6일간(G-6) 각각 복강내-주사하고, diethyl ether 마취하에서 웅성 백서의 간을 부분$(70.4{\pm}1.99%)$-절제하여, 절제 전후의 혈압, 혈장 catecholamine치 및 간 polyamine 함량의 변동을 검토하여 다음의 성적을 얻었다. 1. 백서 꼬리에서 측정한 정상 수축기 혈압은 $98.0{\pm}3.9mmHg$이며, 이는 G-1에 별 영향을 받지 않았으나, G-3, G-5 및 G-6에 의하여는 25% 이상 현저히 저하되었다. 2. 혈장 norepinephrine 및 epinephrine치는 간-부분절제하고 3시간 후에 각각 $20.38{\pm}2.23pmole/ml$ 및 $56.06\pm4.63pmole/ml$로써 현저한 증가를 보였으며 그 증가율은 G-1 및 G-6에 의하여 80.46% 이상 현저히 억제되었다. 3. 간-부분절제 전의 putrescine, spermidine 및 spermine 함량은 각각 $118.6{\pm}14.1$, $873.8{\pm}27.7$ 및 $875.6{\pm}42.1nmole/g$ wet liver로서 절제후 6시간에 각각 5.5배, 1.5배 및 1.3배 이상 증가되었으며, putrescine의 증가만이 G-6에 의하여 유의하게 억제되었을 뿐 guanethidine-전처치에 별 영향을 받지않았다. 이상의 성적으로 미루어 볼 때, 간-부분절제후 재생과정에서 나타나는 polyamine대사의 촉진현상에 교감신경성 catecholamine들이 직접적으로 중요한 역할을 수행한다고 보기는 어렵다.

• The Korean Journal of Physiology and Pharmacology
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• 제1권3호
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• pp.325-335
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• 1997

Evidence for the existance of at least two subclasses of renal adenosine receptors has been presented. N-6-cyclohexyladenosine (CHA) is a relatively selective $A_1$ adenosine agonists, whereas 5'-N-ethylcarboxamidoadenosine (NECA) acts as a preferential agonist of $A_2$ adenoisne receptor. N6-(L-2-phenylisoproryl)-adenosine (PIA) almost unselectively activates both $A_1\;and\;A_2$ adenosine receptors at micromolar concentrations. During the characterization of adenosine receptor in the kidney, we have discovered a novel phenomenon, that is, an intramuscular administration of CHA for 3 days caused a diuresis and a suppression of urinary concentrating ability. To further characterize this novel phenomenon, an intramuscular administration of adenosine and other adenosine angonists, PIA and NECA, and prior treatment of adenosine antagonists, caffeine, theophylline and 1,3-diethyl-8-phenyl-xanthine (DPX) were performed. Systemic administration of CHA, PIA, and NECA for 3 days caused a suppression in heart rate, blood pressure and general motor activity without change in rectal temperature. Systemic administration of CHA, 0.5, 1 and 2 mg/kg/day, for 3 days caused a dose-dependent increase in urine volume and decrease in urinary osmolarity and free water reabsorption. This phenomenon was reversible and repeatable. Administration of adenosine (40 mg/kg/day) produced no apparent effect on the renal function, whereas PIA (2 mg/kg/day) produced an similar effect to CHA on the renal function. Systemic adminstration of NECA, 0.025, 0.05 and 0.25 mg/kg/day, for 3 days caused a dose-dependent increase in urine volume and dose-dependent increases in excreted amount of creatinine, urinary osmolarity and free water reabsorption. These renal effects of adenosine agonist were maximum at second day during the drug administration. In terms of increase in urine volume and the suppression of urinary concentrating ability, NECA was potent than CHA. Prior treatment of caffeine (50 mg/kg/day) or theophylline (50 mg/kg/day) abolished the diuretic effect of CHA, whereas DPX (50 mg/kg/day) did not affect the CHA effect. CHA, 0.5 mg/kg/day, produced no change in plasma renin activity and plasma levels of aldosterone, epinephrine, and norepinephrine. These results suggest that this novel phenomenon produced by an activation of renal adenosine receptors plays an important role in urinary concentrating mechanism.

• The Korean Journal of Physiology
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• 제23권2호
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• pp.363-375
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• 1989

It has been well known that peripheral infusion of angiotensin II results in an increase of blood pressure, and an elevation of aldosterone secretion, and an inhibition of renin relase. However, the direct effect of angiotensin II on renal function has not been clearly established. In the present study, to investigate the effect of angiotensin II on renal function and renin release, angiotensin II (0.3, 3 and 10 ng/kg/min) was infused into a unilateral renal artery of the unanesthetized rabbit and changes in renal function and active and inactive renin secretion rate (ARSR, IRSR) were measured. In addition, to determine the relationship between the renal effect of angiotensin II and adenosine, the angiotensin II effect was evaluated in the presence of simultaneously infused 8-phenyltheophylline (8-PT, 30 nmole/min), adenosine A 1 receptor antagonist. Angiotensin II infusion at dose less than 10 ng/kg/min decreased urine flow, clearances of para-amino-hippuric acid and creatinine, and urinary excretion of electrolytes in dose-dependent manner. The changes in urine flow and sodium excretion were significantly correlated with the change in renal hemodynamics. Infusion of angiotensin II at 10 ng/kg/min also decreased ARSR, but it has no significant effect on IRSR. The change in ARSR was inversely correlated with the change in IRSR. The plasma concentration of catecholamine was not altered by an intarenal infusion of angiotensin II. In the presence of 8-PT in the infusate, the effect of angiotensin II on renal function was significantly attenuated, but that on renin secretion was not modified. These results suggest that the reduction in urine flow and Na excretion during intrarenal infusion of angiotensin II was not due to direct inhibitions of renal tubular transport systems, but to alterations of renal hemodynamics which may partly be mediated by the adenosine receptor.

• 대한한방내과학회지
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• 제22권4호
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• pp.503-512
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• 2001

Objective : This study was carried out to investigate the effects of DDT on the brain damage and hypertension. Methods : We observed the effect of Dodamtang(DDT) extract on KCN-induced coma, focal brain ischemia by MCA occlusion, cytotoxicity and protection of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35). To prove the effect of DDT as a blood pressure depressant, we measured aldosterone, renin activity, catecholamine, sodium and NO density using the seperated blood plasma. Results : DDT showed a protective effect on cytotoxicity of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35) in a dose dependent manner and proved the significant abridgement of brain ischemic area and edema induced by MCA occlusion, a critical decrease of neurologic deficitic grade in the fore-limbs. DDT didn't reduce the duration of KCN(1.87mg/kg iv.)-induced coma and prolonged the survival rate in the case of KCN(3.0mg/kg iv.)-induced coma by the ratio of 20%. While DDT increased the value of NO in SHR, it significantly decreased the blood pressure of SHR and the value of aldosterone& epinephrine in SHR. Conclusions : These results suggested that DDT might be usefully applied for treatment of hypertension, cerebral infarction, and brain damage.

• 운동영양학회지
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• 제16권2호
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• pp.65-71
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• 2012

Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.