• Childhood Kidney Diseases
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• 제16권1호
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• pp.54-57
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• 2012

요로감염환자에서 이차성 거짓저알도스테론증이 발생할 수 있다는 보고들이 흔하지 않게 보고되고 있다. 많은 경우들에서는 요로계통의 기형을 동반하였으나, 요로계기형이 없는 급성 신우신염 환자들에서도 거짓저알도스테론증의 발생이 보고되었다. 대부분의 경우들은 영아에서 발생하였다. 거짓저알도스테론증은 저나트륨혈증, 고칼륨혈증, 그리고 대사성 산증을 특징으로 심할 경우 치명적인 결과를 초래할 수 있다. 더군다나, 본 증례에서와 같이 전해질 불균형에 의한 증세가 식욕부진, 성장장애(failure to thrive) 등으로 미미할 경우 이차성 거짓저알도스테론증의 조기 진단이 어려울 수 있다. 세뇨관 기능이 아직 미숙하고, 요로감염의 발병율이 높은 영아에서는 요로감염으로 진단시 저나트륨혈증, 고칼륨혈증 등의 전해질 불균형의 동반 가능성을 염두에 두어야 할 것으로 사려된다.

• Clinical and Experimental Pediatrics
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• 제49권1호
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• pp.99-102
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• 2006

윌름씨 종양은 주로 1-5세에 복부에 생기는 종양으로 약 25% 이상에서 고혈압을 동반하지만 심각한 고혈압에 의하여 심부전을 보이는 경우는 매우 드물다. 저자들은 3세된 여자 아이가 윌름씨 종양으로 인한 고레닌 혈증으로 다음, 다뇨, 저나트륨성 고혈압과 심부전을 보였으나 수술적으로 종양을 제거한 후 증상 호전을 보였기에 문헌 고찰과 함께 보고하는 바이다.

• 대한한방내과학회지
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• 제32권3호
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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.

• 대한한의학회지
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• 제24권3호
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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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• 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.