• 제목/요약/키워드: Renin

검색결과 260건 처리시간 0.024초

신동맥내 투여한 Angiotensin II가 신장기능 및 Renin 분비에 미치는 영향 (Effect of Unilateral Renal Arterial Infusion of Angiotensin II on Renal Function and Renin Secretion in Unanesthetized Rabbit)

  • 김종훈;강남부;김영진;김선희;조경우
    • 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.

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배 추출 펙틴이 2K1C 고혈압 흰쥐의 혈압, 혈장 Renin, ANP 및 Cardiac Hypertrophy 에 미치는 영향 (The Effect of Pear Pectin on Blood Pressure, Plasma Renin ANP and Cardiac Hypertrophy in Hypertensive Rat Induced by 2K1C)

  • 나창수;윤대환;최동희;김정상;조춘화;은종방
    • 한국식품영양과학회지
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    • 제32권5호
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    • pp.700-705
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    • 2003

  • 배에서 추출된 pectin과 사과에서 추출된 pectin의 3주간 투여가 2K1C 고혈압 흰쥐의 일간 혈압 변화, 혈장 renin, ANP 변화 및 cardiac hypertrophy 변화를 관찰한 결과 다음과 같은 결론을 얻었다. 일간 혈압변화에서 대조군에 비하여 AP-A군의 15일째에 유의한 감소를 보였고, 19일째에 한계적으로 유의한 감소를 나타내었으며, AP-B군의 8일째와 15일째에 유의한 감소를 나타내었으며, AP-C군의 15일째에 한계적으로 유의한 감소를 나타내었다. 또한 대조군에 비하여 PP-A군은 모든 기간 동안 유의성을 나타내지 않았으며, PP-B군의 8일째와 15일째에 유의한 감소를 나타내었으며, PP-C군의 15일째에 유의한 감소를 나타내었다. 혈장 renin변화에 있어서 대조군에 비하여 apple pectin이 투여된 군에서는 모두 유의한 변화가 없었으며, pear pectin이 투여 된 PP-B군에서 한계적으로 유의한 감소를 나타내었다. 혈장 ANP 변화에 있어서 대조군에 비하여 apple pectin이 투여된 군에서는 모두 유의한 변화가 없었으며, pear pectin이 투여된 PP-B군에서 유의한 증가를 나타내었다. Cardiac hypertrophy 변화에 있어서 대조군에 비하여 apple pectin이 투여된 군에서는 모두 유의한 변화가 없었으며, pear pectin이 투여된 PP-C군에서 유의한 감소를 나타내었다.

  • https://doi.org/10.3746/jkfn.2003.32.5.700 인용 PDF KSCI

고혈압(高血壓)에 있어서 Renin-Angiotensin계(系) 및 총교환(總交換) 나트륨에 관(關)한 연구(硏究) (A Study on Renin-Angiotensin System and Total Exchangeable Sodium in Hypertension)

  • 최강원;박정식;이정상;고창순
    • 대한핵의학회지
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    • 제10권1호
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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.

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