• 대한핵의학회:학술대회논문집
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• 1975.06a
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• pp.81.4-82
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• 1975

• 대한핵의학회:학술대회논문집
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• 1977.05a
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• pp.97.2-97.2
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• 1977

• 대한핵의학회:학술대회논문집
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• 1978.06a
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• pp.62.2-63
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• 1978

• 대한핵의학회:학술대회논문집
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• 1978.06a
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• pp.64-64
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• 1978

• 대한핵의학회:학술대회논문집
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• 1976.06a
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• pp.73-73
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• 1976

• 대한핵의학회:학술대회논문집
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• 1979.05a
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• pp.8.1-8.1
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• 1979

• 대한핵의학회:학술대회논문집
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• 1972.11a
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• pp.68.2-68.2
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• 1972

• The Korean Journal of Physiology
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• v.23 no.2
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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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.5
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• pp.700-705
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• 2003

Oriental pear was used as treatment of asthma, control of blood pressure tonic medicine vasoactio, diabetes in oriental medicine. In this study, it was investigated that pear pectin effects on cardiovascular system as blood pressure and renin and atrial natriuretic peptide (ANP) in plasma, cardiac hypertrophy. The experiments were performed on Sprague-Dawley rats, 2K1C hypertension model was prepared by constricting the left renal artery with a sliver clip. Animals were then divided into four groups, 5 mg/kg, 10 mg/kg, 15 mg/kg and the control, pear pectin and apple pectin solutions were supplied with them. The blood pressure was more decreased in pear pectin 10 mg/kg than in apple pectin. The plasma ANP was decreased in pear pectin 10 mg/kg, and renin was increased in same concentration of drug. Cardiac hypertrophy had a tendency to decrease in pear pectin 15 mg/kg, but was not statistically significant compared to control group.

• The Korean Journal of Nuclear Medicine
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• v.10 no.1
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• pp.1-14
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• 1976

The etiologic role of renin-angiotensin system and sodium-volume status in the pathophysiology of various forms of hypertension was investigated. Plasma renin activity (PRA) was measured by radioimmunoassay, while sodium-volume status was evaluated by the determination of total exchangeable sodium(NaE) using isotope dilution method. The subjects consisted of 25 controls, 24 patients with essential hypertension, with chronic renal failure (13 with hypertension, 9 without hypertension) and with malignant hypertension. The results were as follows: 1. An inverse correlation between NaE and PRA was noted in control subjects (r=-0.598, p<0.001) and normal renin essential hypertension(r=-0.551, p<0.05) and the chronic renal failure with hypertension. (r=-0.790, p<0.001) 2. NaE increased markedly the in chronic renal failure with hypertension ($66.9{\pm}8.69mEq/kg$ of LBM, p<0.001) and the chronic renal failure without hypertension ($54.9{\pm}9.28mEq/kg$ of LBM, p<0.05), while mild increase was noted in malignant hypertension ($51.7{\pm}6.24mEq/kg$ of LBM, 0.05$50.1{\pm}7.24mEq$) as well as in its renin subgroups.(p>0.1) 3. Absolute value of PRA was not deviated significantly from control group ($2.53{\pm}1.416ng/ml/hr$) except in malignant hypertension ($6.09{\pm}2.042$, p<0.001). But PRA was inappropriately high in relation to prevailing NaE in the chronic renal failure with hypertension (eleven of thirteen patients) and malignant hypertension (ten of fourteen patients), while PRA variatiation was within physiologic range in the chronic renal failure without hypertension. 4. The NaE-PRA product was markedly increased in the chronic renal failure with hypertension ($514.4{\pm}42.10$, p<0.001) and in malignant hypertension ($442.7{\pm}55.03$, p<0.001), while moderately increased NaE-PRA product was noted in the chronic renal failure without hypertension ($402.6{\pm}59.67$, p<0.001). No significant difference in NaE-PRA product was noted in essential hypertension ($354.4{\pm}62.38$, p>0.1). It is suggested that renin-angiotensin system plays a predominant role in the pathogenesis of malignant hypertension and in hypertension of chronic renal failure, though sodium retention is also contributing factor. PRA variation in essential hypertension does not appear to be associated with any consistent change in Na-volume status, suggesting the existence of another mechanism in the genesis of hypertension and PRA variation.