• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.5
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• pp.471-477
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• 1992

This study was conducted to determine the effect of seaweed ingestion on Na, Ca and K balances in healthy male subjects and to elucidate possible hypolipidemic mechanisms. Six subjects were given a nutritionally controlled diet based on their usual intake for 5-days followed by 5 days in which seaweed was added to the basal diet. Based on the results of the study, the relation between the levels of intake and excretions in stool, urine and serum concentrations was analyzed. In this study, the ingested sodium and potassium were mostly excreted in urine. The highest the rate of urinary excretion to intake for K at 64%, followed by 56% for Na, Conversely, Ca was excreted in stool at higher rates. Analysis of the relation between the intake and excretion in stool revealed that Na and K showed a positive relation with statistical significance. There was no statistically significant relation between the intake and serum concentration of any these minerals. The levels of serum cholesterol and triglyceride were remarkably reduced (p<0.05) by seaweed intake. Thus, the results suggest a beneficial effect of seaweed on Na, Ca, K metabolic control and hypolipidemic mechanism of the healthy male subjects.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.115-121
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• 1990

The interaction between a calcium channel blocker nifedipine and atrial natriuretic peptide (ANP) was examined in normotensive and renal hypertensive rats. The infusion of either ANP or nifedipine produced a significant decrease in mean arterial pressure (MAP). The combined infusion of ANP with nifedipine resulted in a greater fall of MAP than did the infusion of each drug alone. ANP significantly increased urinary volume and excretion of sodium, while nifedipine was without effects. The diuretic/natriuretic effects of ANP were potentiated by the combined infusion with nifedipine. The vasodepressor and renal effects of ANP or nifedipine were qualitatively similar between the normotensive and hypertensive rats. Nifedipine caused an upward and leftward shift of the ANP dose-relaxation curve of the phenylephrine-precontracted thoracic aortic rings isolated from the normotensive rats , suggesting that the vasodilation sensitivity to ANP is increased in the presence of nifedipine. These results indicate that nifedipine enhances the vasodepressor effect of ANP, the likely mechanisms being attributable to a contraction of effective intravascular volume as a consequence of potentiated renal excretion and a greater peripheral vasodilation.

• The Korean Journal of Pharmacology
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• v.12 no.1
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• pp.31-44
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• 1976

It has been reported that many of the effects of digitalis glycosides could be mediated partly through the central nervous system. In this study the effects of ouabain given directly into the lateral ventricle of the brain on the renal function of the rabbit were investigated. Intraventricular ouabain elicited antidiuresis in doses ranging from 0.1 to $3\;{\mu}g$, exhibiting a rough dose-response relationship, and decreased the renal plasma flow, glomerular filtration rate and urinary excretion of sodium and potassium, concomitant with the decrease of urine flow. These decreases in urine flow, excretory rate of electrolytes significantly correlated with the decrease in renal plasma flow or glomerular filtration rate, suggesting that the antidiuresis might have been induced by the hemodynamic changes. Intravenous ouabain in a dose of $1\;{\mu}g$ did not affect the renal function. Systemic blood pressure as well as cardiac activity was not affected by the intraventricular ouabain. Effects of the intraventricular ouabain on renal function were abolished by the intravenous phentolamine-pretreatment but not affected by intraventricular phentolamine-pretreatment. Neither vasopressin infusion nor hydration did affect the renal effects of intraventricular ouabain. From these observations, it is suggested that the antidiuresis of intraventricular ouabain is induced by the increased sympathetic influence to the kidney.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.403-411
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• 1997

To elucidate the mechanism of gentamicin induced renal dysfunction, renal functions and activities of various proximal tubular transport systems were studied in gentamicin-treated rats (Fisher 344). Gentamicin nephrotoxicity was induced by injecting gentamicin sulfate subcutaneously at a dose of 100 $mg/kg{\cdot}day$ for 7 days. The gentamicin injection resulted in a marked polyuria, hyposthenuria, proteinuria, glycosuria, aminoaciduria, phosphaturia, natriuresis, and kaliuresis, characteristics of aminoglycoside nephropathy. Such renal functional changes occurred in the face of reduced GFR, thus tubular transport functions appeared to be impaired. The polyuria and hyposthenuria were partly associated with a mild osmotic diuresis, but mostly attributed to a reduction in free water reabsorption. In renal cortical brush-border membrane vesicles isolated from gentamicin-treated rats, the $Na^+$ gradient dependent transport of glucose, alanine, phosphate and succinate was significantly attenuated with no changes in $Na^+-independent$ transport and the membrane permeability to $Na^+$. These results indicate that gentamicin treatment induces a defect in free water reabsorption in the distal nephron and impairs various $Na^+-cotransport$ systems in the proximal tubular brush-border membranes, leading to polyuria, hyposthenuria, and increased urinary excretion of $Na^+$ and other solutes.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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• pp.337-341
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• 2006

The present study was designed to investigate the protein expression of nitric oxide synthase (NOS) and guanylyl cyclase (GC) activity in ischemia/perfusion (I/R) renal injury in rats. Renal I/R injury was experimentally induced by clamping the both renal pedicle for 40 min in Sprague-Dawley male rats. The renal expression of NOS isoforms was determined by Western blot analysis, and the activity of guanylyl cyclase was determined by the amount of guanosine 3', 5'-cyclic monophosphate (cGMP) formed in response to sodium nitroprusside (SNP), NO donor. I/R injury resulted in renal failure associated with decreased urine osmolality. The expression of inducible NOS (iNOS) was increased in I/R injury rats compared with controls, while endothelial NOS (eNOS) and neuronal NOS (nNOS) expression was decreased. The urinary excretion of NO metabolites was decreased in I/R injury rats. The cGMP production provoked by SNP was decreased in the papilla, but not in glomerulus. These results indicate an altered regulation of NOS expression and guanylyl cyclase activity in I/R-induced nephropathy.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.5
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• pp.1201-1209
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• 2007

The present study was designed to examine whether water extract of Acanthopanacis cortex(AC) has an effect on renal functional parameters in association with the expression of aquaporin 2 (AQP-2) and heme oxygenase-1 (HO-1) in the ischemia/reperfusion induced acute renal failure (ARF) rats. Polyuria caused by down-regulation of renal AQP 2 in the ischemia-induced ARF rats was markedly restored by administration of AC (200 mg/kg, p.o.) with restoring expression of AQP 2 in the kidney. Administration of AC lowered the renal expression of HO-1, which was upregulated in rats with ischemia/reperfusion-induced ARF. The renal functional parameters including creatinine clearance, urinary sodium excretion, urinary osmolality, and solute-free reabsorption were also markedly restored in ischemia-ARF rats by administration of AC. Histological study also showed that renal damages in the ARF rats were abrogated by administration of AC. Taken together, the present data indicate that AC ameliorates renal defects in rats with ischemia/reperfusion-induced ARF.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.683-693
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• 2001

This study was attempted to investigate the effect of raclopride, a dopamine $D_2$ receptor antagonist, on renal function in dog. Raclopride (70-220$\mu\textrm{g}$/kg), when given intravenously, Produced antidiuresis along with the decrease in free water clearance ( $C_{H_2O}$), urinary excretion of sodium and potassium ( $E_{Na}$ , $E_{K}$), partially decreased osmolar clearance ( $C_{osm}$) and increased reabsorption rates of sodium and potassium in renal tubules ( $R_{Na}$ , $R_{K}$). Raclopride administered into a renal artery did not influence on renal function in small doses (10 and 30$\mu\textrm{g}$/kg), whereas exhibited the decrease of urine volume (Vol) and $C_{H_2O}$ both in experimental and control kidney in much dose (100$\mu\textrm{g}$/kg), at this time, the decreased rates of both Vol. and $C_{H_2O}$) were more prominent in control kidney rather than that elicited in experimental kidney, and then only via was decreased in control kidney but increased in experimental kidney. Raclopride administered via carotid artery (30-200$\mu\textrm{g}$/kg) did not influence at all on renal function. Antidiuretic action induced by raclopride given intravenously was not affected by renal denervation. Raclopride given into carotid artery was little effect on renal function without relation to renal denervation. Above results suggest that raclopride produces antidiuresis by potentiation of antidiuretic hormone (ADH) action in blood without increase of ADH secretion in posterior pituitary gland, it is not related to renal nerve function in dogs.ogs.s.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.5
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• pp.273-277
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• 2011

Nitric oxide (NO) and atrial natriuretic peptide (ANP) may induce vascular relaxation by increasing the production of cyclic guanosine monophosphate (cGMP), an important mediator of vascular tone during sepsis. This study aimed to determine whether regulation of NO and the ANP system is altered in lipopolysaccharide (LPS)-induced kidney injury. LPS (10 $mg{\cdot}kg^{-1}$) was injected in the tail veins of male Sprague-Dawley rats; 12 hours later, the kidneys were removed. Protein expression of NO synthase (NOS) and neutral endopeptidase (NEP) was determined by semiquantitative immuno-blotting. As an index of synthesis of NO, its stable metabolites (nitrite/nitrate, NOx) were measured using colorimetric assays. mRNA expression of the ANP system was determined by real-time polymerase chain reaction. To determine the activity of guanylyl cyclase (GC), the amount of cGMP generated in response to sodium nitroprusside (SNP) and ANP was calculated. Creatinine clearance decreased and fractional excretion of sodium increased in LPS-treated rats compared with the controls. Inducible NOS protein expression increased in LPS-treated rats, while that of endothelial NOS, neuronal NOS, and NEP remained unchanged. Additionally, urinary and plasma NOx levels increased in LPS-treated rats. SNP-stimulated GC activity remained unchanged in the glomerulus and papilla in the LPS-treated rats. mRNA expression of natriuretic peptide receptor (NPR)-C decreased in LPS-treated rats, while that of ANP and NPR-A did not change. ANP-stimulated GC activity reduced in the glomerulus and papilla. In conclusion, enhancement of the NO/cGMP pathway and decrease in ANP clearance were found play a role in the pathogenesis of LPS-induced kidney injury.

• 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.

• Nutrition Research and Practice
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• v.9 no.4
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• pp.385-392
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• 2015

BACKGROUND/OBJECTIVES: Recent studies have reported an association of the angiotensin II type 2 receptor (AT2R) 3123Cytosine/Adenine (3123C/A) polymorphism with essential hypertension and cardiovascular diseases. The purpose of the study was to investigate whether the AT2R 3123C/A polymorphism affects blood pressure for free-living hypertensive men during a 5-month intervention period. SUBJECTS/METHODS: The subjects were free-living hypertensive Japanese men aged 40 to 75 years who agreed to intervention in the period from 2004 to 2011. Detection of the AT2R 3123C/A polymorphism was determined by polymerase chain reaction. The dietary intervention was designed to decrease salt level and to increase potassium level through cooking instructions and self-monitoring of the diet. The exercise session consisted of activities such as stretching, resistance training, and walking. Blood pressure, urinary sodium and potassium excretion, dietary and lifestyle data, and non-fasting venous blood sample were collected at baseline and after the intervention period. RESULTS: Thirty nine subjects were eligible for participation and the follow-up rate was 97.4%. The C allele proportion was 57.9%. AT2R 3123C/A polymorphism was X-chromosome-linked, therefore we analyzed the C and A genotypes. At baseline, no significant differences were observed between the genotype groups. After the intervention, there were no significant differences in lifestyle habit between the groups. Nevertheless, the estimated salt excretion (g/day) was significantly decreased only in the C genotype (13.0-10.3, P = 0.031). No significant change was observed in systolic blood pressure (SBP) (mmHg) in the A genotype, but a significant decrease was observed in the C genotype (150.0-141.5, P = 0.024). CONCLUSTIONS: In the C genotype, it might be easy to improve SBP through lifestyle intervention in free-living hypertensive Japanese men, however generalization could not be achieved by the small sample size.