• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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• pp.343-347
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• 2006

The present study was designed to investigate the effects renin-angiotensin-aldosterone system (RAAS), endothelin (ET) and local natriuretic peptide (NP) system for glomerulopathy induced in the experimental bilateral ureteral obstructive rats. Sprague-Dawley male rats ($200{\sim}220g$ body weight) were bilaterally obstructed by ligation of the proximal ureters for 24 hours. Control rats were treated in the same ways, except that no ligature was made. The glomeruli were isolated from cortex by graded sieve methods, and the mRNA expressions of local renin-angiotensin system (RAS), aldosterone synthase (CYP11B2), endothelin-1 (ET-1) and NP system were determined by real-time polymerase chain reaction. Following the bilateral ureteral obstruction, the mRNA expressions of renin, angiotensin converting enzyme 1 as well as ET-1 were increased, while that of angiotensin converting enzyme 2 was not changed. The expressions of CYP11B2 and angiotensin II receptors were not changed. C-type natriuretic peptide (CNP) expression was increased, while its receptors (natriuretic peptide receptor-B) were not changed. We suggest that the upregulation of local RAS and ET playa role in the progressive glomerular injury, and that the enhanced CNP activity also plays a compensatory role in obstructive uropathy in the glomerulus.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.155-155
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• 2001

Acute cadmium exposure has been shown to increase sodium reabsorption in kidney through increase in aldosterone secretion in human and rodents. However, the antinatriuresis is not completely explained by hyperaldosteronism. Moreover, it is still controversial that the increase in plasma aldosterone concentration is mediated by the renin-angiotensin-aldosterone system(RAAS).(omitted)

• 대한핵의학회:학술대회논문집
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• 1973.11a
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• pp.62.2-62.2
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• 1973

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.319-328
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• 2020

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.189-202
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• 1985

Enhanced activity of renin-angiotensin-aldosterone system has been suggested as a cause of the high blood pressure in certain forms of experimental hypertension. In spontaneously hypertensive rats, however, increased activity of the system has not been found, and even suppressed renin angiotensin system has been reported in the spontaneously hypertensive rat. In the present experiments it was attempted to explore the possible alteration of the short loop negative feedback control in the hypertensive rat. Experiments have been done in the anesthetized spontaneously hypertensive rats(SHR) as well as in normotensive Wistar and Sprague Dawley rats as control. Responses of the plasma renin activity to the intravenous L-isoproterenol were dose dependent, in both SHR and normotensive control rats. Hypotensive responses to smaller do sea of L-isoproterenol were more accentuated in SHR than in the normotensive control rats. Angiotensin If given intravenously suppressed plasma renin activity in a dose dependent fashion in both groups. However, these suppressive responses were significantly attenuated in SHR as compared with the normotensive control rats. Treatment with angiotensin I-converting enzyme inhibitor did not correct the attenuated responses of the plasma renin activity to angiotensin II in SHR. Intravenous infusion of arginine vasopressin also produced a dose-dependent suppression of plasma renin activity in both groups. The responses to arginine vasopressin were also significantly attenuated to the normotensive control rats. In the sodium-depleted SHR, arginine vasopressin did not suppress plasma renin activity, whereas the suppressive responses to arginine vasopressin in the normotensive control rats were not different from the untreated control rats. These data suggest that there may be a derangement in the short loop negative feedback control of the renin-angiotensin system in spontaneously hypertensive rat.

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

• 한국체육학회지인문사회과학편
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• v.55 no.2
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• pp.603-615
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• 2016

This study was conducted by performing intensities aerobic exercise for 12 weeks, three times a week targeting 28 middle aged women. The purpose of this study was analyzing factors which affect cognitive function and changes of blood pressure, renin-aldosterone system, neurotransmitter, cognitive function and working memory after treatment. The participants were divided into three groups which are the control group(n=9, non exercise), moderate intensity aerobic exercise group(n=10, 50%V02max), high intensity aerobic exercise group(n=9, 70%V02max). The two-way ANOVA(repeated measure) and multiple regression analysis were carried out to target those three groups before and after treatment. The results were as follows like this. The moderate intensity aerobic exercise increased renin, brain derived neurotrophic factor(BDNF), cognitive function and working memory. Also, it reduced aldosterone, angiotensinII and aldosterone-renin ratio. The high intensity aerobic exercise showed increase BDNF, cognitive function and working memory and decrease systolic. As a result of a multiple regression analysis of factors affecting cognitive function after intensities aerobic exercise, the moderate intensity aerobic exercise affected diastolic blood pressure, decrease of aldosterone-renin ratio and working memory. Also, an increase of BDNF affected cognitive function, the high intensity aerobic exercise affected working memory BDNF and an increase of serotonin affected cognitive function. Therefore, It could be seen that more than moderate intensity exercise increase woman's cognitive function and working memory. Also, there were metabolic factors which affect the increase of cognitive function. To moderate intensity exercise, renin-aldosterone and working memory affected to increase of cognitive function. For high intensity exercise, BDNF and working memory affected to it.

• Nutrition Research and Practice
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• v.11 no.5
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• pp.388-395
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• 2017

BACKGROUND/OBJECTIVES: Although Korean fermented foods contain large amounts of salt, which is known to exacerbate health problems, these foods still have beneficial effects such as anti-hypertension, anti-cancer, and anti-colitis properties. We hypothesized that ganjang may have different effects on blood pressure compared to same concentrations of salt. MATERIALS/METHODS: Sprague-Dawley rats were divided into control (CT), NaCl (NC), and ganjang (GJ) groups and orally administered with 8% NaCl concentration for 9 weeks. The systolic blood pressure (SBP), serum chemistry, $Na^+$ and $K^+$ concentrations and renal gene expressions were measured. RESULTS: The SBP was significantly increased in the NC group compared to the GJ and CT groups. In addition, the $Na^+$ concentration in urine was higher in the GJ and NC groups than the CT group, but the urine volume was increased in the GJ group compared to the other groups. The serum renin levels were decreased in the GJ group compared to the CT group, while the serum aldosterone level was decreased in the GJ group relative to the NC group. The mRNA expression of the renin, angiotensin II type I receptor, and mineralocorticoid receptor were significantly lower in the GJ group compared to other groups. Furthermore, GJ group showed the lowest levels of genes for $Na^+$ transporter in kidney cortex such as $Na^+/K^+$ $ATPase{\alpha}1$ ($NKA{\alpha}1$), $Na^+/H^+$ exchanger 3 (NHE3), $Na^+/HCO_3{^-}$ co-exchanger (NBC), and carbonic anhydrases II (CAII). CONCLUSIONS: The decreased SBP in the GJ could be due to decreased renin and aldosterone levels in serum and increased urinary volume and excretion of $Na^+$ with its transporter gene alteration. Therefore, ganjang may have antihypertensive effect despite its high contents of salt.

• Korean Circulation Journal
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• v.53 no.9
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• pp.606-618
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• 2023

Background and Objectives: The prognostic or safety implication of renin-angiotensin-aldosterone system inhibitors (RASi) in hypertrophic cardiomyopathy (HCM) are not well established, mainly due to concerns regarding left ventricular outflow tract (LVOT) obstruction aggravation. We investigated the implications of RASi in a sizable number of HCM patients. Methods: We enrolled 2,104 consecutive patients diagnosed with HCM in 2 tertiary university hospitals and followed up for five years. RASi use was defined as the administration of RASi after diagnostic confirmation of HCM. The primary and secondary outcomes were all-cause mortality and hospitalization for heart failure (HHF). Results: RASi were prescribed to 762 patients (36.2%). During a median follow-up of 48.1 months, 112 patients (5.3%) died, and 94 patients (4.5%) experienced HHF. Patients using RASi had less favorable baseline characteristics than those not using RASi, such as older age, more frequent history of comorbidities, and lower ejection fraction. Nonetheless, there was no difference in clinical outcomes between patients with and without RASi use (log-rank p=0.368 for all-cause mortality and log-rank p=0.443 for HHF). In multivariable analysis, patients taking RASi showed a comparable risk of all-cause mortality (hazard ratio [HR], 0.70, 95% confidence interval [CI], 0.43-1.14, p=0.150) and HHF (HR, 1.03, 95% CI, 0.63-1.70, p=0.900). In the subgroup analysis, there was no significant interaction of RASi use between subgroups stratified by LVOT obstruction, left ventricular (LV) ejection fraction, or maximal LV wall thickness. Conclusions: RASi use was not associated with worse clinical outcomes. It might be safely administered in patients with HCM if clinically indicated.