• The Korean Journal of Physiology
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• v.8 no.1
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• pp.7-14
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• 1974

This study was carried out to investigate the acute changes in R-A-A system following lasix administration, and to evaluate the materials in plasma R-A-A system and electrolytic excretion every 30 minutes for 2 hours after lasix administration with normal high sodium Korean food, moderate sodium restriction, and severe sodium restriction, and it was concluded as followed; 1. Plasma renin activity, angiotensin II concentration, and aldosterone concentration elevated in course of time after lasix administration with high sodium Korean food, but the R-A-A system takes insignificant part because of the increasing rate was so slight. 2. Although the increasing rate of plasma renin activity reached lower levels, angiotensin II and aldosterone concentration were significantly increased after lasix administration with moderate sodium restriction. 3. It was observed that higher rise in aldosterone concentration following lasix administration during severe sodium restriction than when moderate sodium restriction. 4. Urinary sodium and potassium excretion during two hours after lasix administration showed decrease as little as the amount of sodium intake, but K/Na excretion ratio showed increase with small amount of sodium intake because of the decreasing rate of potassium was low value. 5. Sodium excretion after lasix administration reached more than 1.5 times of sodium intake, even though R-A-A reaction showed significantly. 6. As our results showed, R-A-A reaction following acute diuresis was insignificant with high sodium Intake, the increasing ratio of aldosterone concentration showed high rise compare with of plasma renin activity as little as the amount of sodium intake, and the participated rate in sodium reabsorption of R-A-A system was increased.

• 대한핵의학회:학술대회논문집
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• 1975.06a
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• pp.81.3-81.3
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• 1975

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.173-187
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• 1985

Renal compensatory adaptation caused by ablation of a part of renal mass has long been known in the field of the compensatory renal hypertrophy or hyperplasia. Many reports were found on the chronic mechanisms on the compensatory renal hyperfunction after exclusion of the contralateral kidney. However the mechanism(s) of the acute compensatory hyperfunction after contralateral exclusion has not yet been clarified. In the present experiment, we have tried to prove the possibility of the involvement of the renin-angiotensin system and/or prostaglandin system in the control mechanism of the acute compensatory renal hyperfunction after contralateral kidney exclusion. There were found different responses of the renal hyperfunction by contralateral renal pedicle or ureteral occlusion. Contralateral renal pedicle or ureteral occlusion caused a sustained increases of the urinary volume, sodium and potassium excretion, while the magnitude of the changes was different quantitatively by the maneuvers. Blood collection affected on the acute compensatory renal responses after ureteral as well as renal pedicle occlusion. Plasma prostaglandin $E_2$ level was not changed by the contralateral renal pedicle or ureteral occlusion. Urinary excretion of Prostaglandin $E_2$, the indices of renal prostaglandin biosynthesis, was not changed by the contralateral renal pedicle occlusion, but increased without significance by the contralateral ureteral occlusion. Acute renal compensatory responses after contralateral renal pedicle occlusion were blocked by the pretreatment of indomethacin. Plasma renin activity increased after contralateral ureteral occlusion, but the pattern of the increases was the same as in the time-control group. Plasma renin activity after contralateral renal pedicle occlusion did not change by the time sequence. SQ 20,881, an angiotensin I converting enzyme inhibitor, blunted the contralateral renal responses after the renal pedicle occlusion. Bilateral renal denervation abolished the contralateral renal responses after the renal pedicle occlusion. The above data suggest that there is no direct evidence to support the involvement of the renin-angiotensin system and/or prostaglandin system for the acute compensatory renal hyperfunction after contralateral kidney exclusion, and that the functional changes of the intact kidney may be caused by a humoral substances, or other mechanisms by afferent renal nerve activity originating from the treated kidney.

• Clinical and Experimental Pediatrics
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• v.64 no.3
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• pp.121-122
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• 2021

• Korean Circulation Journal
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• v.53 no.9
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• pp.619-620
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• 2023

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.4
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• pp.299-307
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• 2015

Severe acute pancreatitis (SAP) is normally related to multiorgan dysfunction and local complications. Studies have found that local pancreatic renin-angiotensin system (RAS) was significantly upregulated in drug-induced SAP. The present study aimed to investigate the effects of angiotensin II receptors inhibitor valsartan on dual role of RAS in SAP in a rat model and to elucidate the underlying mechanisms. 3.8% sodium taurocholate (1 ml/kg) was injected to the pancreatic capsule in order for pancreatitis induction. Rats in the sham group were injected with normal saline in identical locations. We also investigated the regulation of experimentally induced SAP on local RAS expression in the pancreas through determination of the activities of serum amylase, lipase and myeloperoxidase, histological and biochemical analysis, radioimmunoassay, fluorescence quantitative PCR and Western blot analysis. The results indicated that valsartan could effectively suppress the local RAS to protect against experimental acute pancreatitis through inhibition of microcirculation disturbances and inflammation. The results suggest that pancreatic RAS plays a critical role in the regulation of pancreatic functions and demonstrates application potential as AT1 receptor antagonists. Moreover, other RAS inhibitors could be a new therapeutic target in acute pancreatitis.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.253-258
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• 2001

The present study was aimed to examine whether the expression of renin is associated with that of cyclooxygenase-2 (COX-2) in the kidney. Male Sprague-Dawley rats were made two-kidney, one clip (2K1C) or deoxycorticosterone acetate (DOCA)-salt hypertensive, to stimulate or to inhibit the endogenous renin-angiotensin system, respectively. The expression of renin and COX-2 mRNA was determined in the cortex of the kidney by reverse transcription-polymerase chain reaction. 2K1C hypertensive rats showed an increased expression of renin as well as of COX-2 in the clipped kidney. The expression of renin was decreased in parallel with that of COX-2 in the contralateral non-clipped kidney. Removal of the renal arterial clip reversed the expression of both genes, along with the blood pressure, to the control level. On the other hand, DOCA-salt hypertension was associated with parallel decreases of renin and COX-2 expression. These results indicate that renin and COX-2 genes are coordinately expressed in the kidney.

• Proceedings of the Zoological Society Korea Conference
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• 1996.10a
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• pp.217.1-217
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• 1996

No Abstract, See Full Text

• Nutrition Research and Practice
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• v.17 no.2
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• pp.192-205
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• 2023

BACKGROUND/OBJECTIVES: It is known that the renin-angiotensin system (RAS) in the brain could regulate cognitive functions as well as blood pressure. Inhibition of RAS for the improvement of cognitive function may be a new strategy, but studies so far have mostly reported on the effects of RAS inhibition by drugs, and there is no research on cognitive improvement through RAS inhibition of food ingredients. Therefore, this study investigated the effect of curcumin on blood pressure and cognitive function and its related mechanism in spontaneously hypertensive rat/Izm (SHR/Izm). MATERIALS/METHODS: Six-week-old SHR/Izm rats were divided into 5 groups: control group (CON), scopolamine group (SCO, drug for inducing cognitive deficits), positive control (SCO and tacrine [TAC]), curcumin 100 group (CUR100, SCO + Cur 100 mg/kg), and curcumin 200 group (CUR200, SCO + Cur 200 mg/kg). Changes in blood pressure, RAS, cholinergic system, and cognitive function were compared before and after cognitive impairment. RESULTS: The SCO group showed increased blood pressure and significantly reduced cognitive function based on the y-maze and passive avoidance test. Curcumin treatments significantly improved blood pressure and cognitive function compared with the SCO group. In both the CUR100 and CUR200 groups, the mRNA expressions of angiotensin-converting enzyme (ACE) and angiotensin II receptor type1 (AT1), as well as the concentrations of angiotensin II (Ang II) in brain tissue were significantly decreased. The mRNA expression of the muscarinic acetylcholine receptors (mAChRs) and acetylcholine (ACh) content was significantly increased, compared with the SCO group. CONCLUSIONS: The administration of curcumin improved blood pressure and cognitive function in SCO-induced hypertensive mice, indicating that the cholinergic system was improved by suppressing RAS and AT1 receptor expression and increasing the mAChR expression.