• Childhood Kidney Diseases
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• v.16 no.1
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• pp.54-57
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• 2012

A 6-month-old boy with vesicoureteral reflux exhibited features of transient type 1 pseudohypoaldosteronism (PHA) in the course of urinary tract infection. PHA presents hyponatremia, hyperkalemia, and metabolic acidosis, accompanying with high urinary sodium, low potassium excretion, and high plasma aldosterone concentration. Severe electrolyte disturbance can occur in an infant with vesicoureteral reflux because of secondary PHA. Appropriate treatment of dehydration and sodium supplementation induces rapid improvement of electrolyte imbalance and metabolic acidosis resulting from secondary PHA associated with vesicoureteral reflux.

• Clinical and Experimental Pediatrics
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• v.49 no.1
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• pp.99-102
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• 2006

A 3-year-old girl presented with polydipsia, polyuria, hyponatremia, hypertension and congestive heart failure. Her polyuria was unresponsive to water restriction and vasopressin challenge tests, and her blood pressure was not effectively controlled by antihypertensive drugs. Radiologic examinations revealed a Wilms' tumor in the right kidney. Her plasma renin activity and aldosterone concentration were greatly increased. After surgical removal of the tumor, the congestive heart failure disappeared. Congestive heart failure due to Wilms' tumor is very rare and we report here on such a case, with a brief review of the literature.

• The Journal of Internal Korean Medicine
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• v.32 no.3
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• pp.345-360
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• 2011

Objectives : This study was examined to investigate the effects of Cheonmagudeng-um gagam (CGG) extract on spontaneous hypertension. Methods : For the study of CGG, we divided rats into three groups. The normal group was Wister Kyoto rats (WKY). The control group was spontaneously hypertensive rats (SHR). The treatment group was SHR which were administered CGG extract (SHR-CGG). SHR-CGG were orally administered CGG extract that was diluted in distilled water at the various concentrations for 4 weeks (234.5 mg/kg) and SHR were orally administered the same dosage of plain distilled water as SHR-CGG. Then we measured anti-oxygen effects, ACE inhibitory activity, weight of heart and kidney, blood pressure, heart rate, plasma aldosterone, electrolyte, creatinine, uric acid, BUN, and observed the cortex of the cardiac muscle, kidney, and adrenal gland. Results : CGG increased DPPH scavenging activity and SOD similar activity depending on the concentration. CGG significantly decreased ROS, TNF-${\alpha}$, IL-6, IL-$1{\beta}$, heart weight, blood pressure, heart rate, aldosterone, and BUN in SHR. CGG increased ACE inhibition activity depending on the concentration. CGG inhibited the heart, kidney and adrenal gland tissue injury that is caused by hypertension. Conclusions : These results suggest that CGG is effective in treatment and prevention of hypertension.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.72-83
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• 2003

Objective : The goal of the present study was to investigate the protective effect of Gamiheechum-tang (Jiaweixiqian-tang; GHCT) on brain tissue damage from chemical or ischemic insults. Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GHCT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : Animal groups treated with GBCT showed significantly decreased hypertension, and reduced levels of aldosterone, dopamine, and epinephrine in the plasma. GHCT treatments ($l0-200\mu\textrm{g}/ml$) significantly decreased cultured cortical neuron death mediated by AMPA, kainate, BSO, or Fe2+ when measured by LDH release assay. Yet, cell death mediated by NMDA was effectively protected by GHCT at the highest concentration examined ($200\mu\textrm{g}/ml$). In the in vivo experiment examining brain damage by MCA occlusion, affected brain areas by ischemic damage and edema were significantly less in animal groups administered with GHCT compared to the non-treated control group. Neurological examinations of forelimbs and hindlimbs showed that GHCT treatment improved animals' recovery from ischemic injury. Moreover, the extent of injury in cortical and hippocampal pyramidal neurons in ischemic rats was much reduced by GHCT, whose morphological features were similarly observed in non-ischemic animals. Conclusion : The present data suggest that GBCT may play an important role in protecting brain tissues from chemical or ischemic injuries.

• 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.