• The Korean Journal of Pharmacology
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• v.12 no.2 s.20
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• pp.43-49
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• 1976

The facts that $PGE_2$ produced diuresis in the rabbit when given into a lateral ventricle of the brain and that $PGF_{2{\alpha}}$ is abundantly found in the brain prompted us to investigate the effects of $PGF_{2{\alpha}}$ introduced directly into the ventricle on the renal function. $PGF_{2{\alpha}}$ given intraventriculary in doses of $10{\mu}g\;and\;100{\mu}g$ elicited prompt diuresis, 10-fold increase of sodium excretion and two-fold increment of potassium excretion. Free water reabsorption also increased along with the increased osmolar clearance. Neither renal plasma flow nor glomerular filtration rate did change significantly. This, along with the fact that the percentage of reabsorbed sodium filtered decreased from 99.5 to 93.9, indicates the tubular site of the diuretic and natriuretic action. Atropine pretreatment did not influence the renal effects of intraventricular $PGF_{2{\alpha}}$. Intravenously administered $PGF_{2{\alpha}}$ in doses of 30 to $100{\mu}g$ did not produce any significant change in renal function. Intraventricular $PGF_{2{\alpha}}$ had no effect on the systemic blood pressure, whereas intravenous administration brought about a transient hypotension. These observations suggest that $PGF_{2{\alpha}}$ induces diuresis and natriuresis via central mechanism, that the site of the action resides in renal tubules, and that the reabsorption of sodium is inhibited in the proximal tubule, possibly through mediation of certain humoral agent. Overall, it is suggested that $PGF_{2{\alpha}}$ might play a roll in regulating renal function through the center.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.201-210
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• 1987

수온변화에 따른 심맥관계 및 신장기능의 변화와 생체실험을 통한 온도에 의한 adrenoceptor의 변형을 알아보기 위해, 무마취 자라에서 $18^{\circ}C$에서 $25^{\circ}C$로 수온을 증가시 나타나는 혈압, 심박동수 및 신장기능의 변화를 관찰하고, epinephrine 1 ug/kg과 10 ug/kg을 상이한 온도에 노출된 자라의 정맥내 투여하여 나타나는 효과를 비교하였다. 1) $18^{\circ}C$에서 $25^{\circ}C$로 수온을 증가시킴에 따라 심박동수는 현저히 증가하여 일정하게 유지되었으나, 혈압 및 혈장 renin 활성도는 변화하지 않았다. 온도증가에 의해 뇨량, 사구체여과율 및 전해질 배설량의 현저한 증가를 보였으나 90분부터는 서서히 감소하기 시작하였다. 2) 수온 $18^{\circ}C$에 노출된 자라에서 epinephrine은 dose-dependent한 양상으로 혈압 및 심박동수를 증가시켰으며, 다량의 epinephrine 투여시 작용시간은 현저히 연장되어 있었다. $25^{\circ}C$에 노출된 자라에서는 epinephrine에 의한 혈압상승 효과 및 심박동수 증가는 나타났으나, dose dependency나 작용시간의 차이는 발견할 수 없었다. 3) 동량의 epinephrine에 의한 혈압 및 심박동수의 증가효과는 $18^{\circ}C$와 $25^{\circ}C$에 노출된 자라에서 유의한 차이를 발견할 수 없었으나, $18^{\circ}C$에 노출된 자라에서 epinephrine의 작용시간 및 반감기가 현저히 연장되어 있었다. 4) Epinephrine 투여에 의해 뇨량, 사구체여과율 및 전해질 배설량의 증가를 관찰하였으며, 이는 dose-dependent 양상이었다. 그러나, 신장효과의 유의한 차이는 상이한 온도에 노출된 두 군에서 발견할 수 없었다. 이상의 결과로, 온도증가에 의한 이뇨 및 sodium 배설효과는 혈관이완에 의한 사구체여과율의 증가에 기인한 것으로 사료되며, 상이한 온도에 노출된 자라에서 epinephrine 효과의 차이를 발견할 수 없었던 것은 본 실험에서 가한 좁은 범위의 온도의 변화 내에서는 adrenoceptor의 변형이 나타나지 않을 것이라고 추론하였다. 그러나 저온에서의 epinephrine의 작용시간의 연장은 아마도 epinephrine의 파괴 효소의 활성도의 감소인 것으로 사료된다.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.291-296
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• 1987

There have been reports on the aberration of the control mechanisms of the blood pressure, hormone secretion, and renal functions in spontaneously hypertensive rats (SHR). However, the contribution of the renin-angiotensin system in the maintenance of high blood pressure in SHR is still controversial. Recently, it has been reported that the negative feedback short loop control mechanism of the renin-angiotensin system may be changed in SHR. In the present experiment, it was attempted to explore the possible alterations in the effect of arginine vasopressin (AVP) on the renal function in SHR. Experiments have been done in anesthetized SHR as well as in normotensive Wistar and Sprague-Dawley rats as control groups. Pharmacologic doses of AVP (10-13 mU/rat/10 min) decreased urine volume, excreted amount of creatinine and para-amino-hippuric acid. No differences in these parameters was observed between normotensive and hypertensive rats. AVP increased sodium and potassium excretion, but the responses in SHR were suppressed as compared with normotensive rats. Intravenous infusion of AVP also increased blood pressure in normotensive and hypertensive rats and a vasopressor effect of AVP was attenuated in SHR. There was a positive correlation between the changes in blood pressure and excreted amount of sodium during AVP infusion. These data suggest that the attenuated natriuretic effect of intravenous infusion of AVP may be due to a difference in renal tubular responsiveness to AVP but not due to a difference in vasopressor responsiveness.

• Tuberculosis and Respiratory Diseases
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• v.59 no.3
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• pp.306-310
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• 2005

Hyponatremia which is due to excessive sodium loss in the urine and decrease in extracellular fluid volume following an acute or chronic central nervous system injury, has been conjunctively described as cerebral salt wasting syndrome (CSWS). This syndrome is often confused with dilutional hyponatremia due to inappropriate secretion of antidiuretic hormone. Accurate diagnosis and management are mandatory for improvement of the course of the disease. This report describes a case of a 31-year-old male patient with CSWS associated with tuberculous meningitis. The patient exhibited hyponatremia, polyuria, excessive natriuresis, volume depletion, and hypotension. He was diagnosed to manifest CSWS and was treated by administration of fluids, salt, and fludrocortisone. After the respective treatments, symptoms of polyuria and hypotension were gradually resolved and hyponatremia was corrected.

• Childhood Kidney Diseases
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• v.24 no.1
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• pp.42-46
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• 2020

Disturbances in water and salt balances are relatively common in children after brain tumor surgery. However, the coexistence of different diseases of water and sodium homeostasis is challenging to diagnose and treat. The coexistence of combined central diabetes insipidus (CDI) and cerebral salt wasting syndrome (CSWS) is rare and may impede accurate diagnosis. Herein, we report the case of an 18-year-old girl who underwent surgery for a germinoma and who presented prolonged coexistence of CDI and CSWS. The patient was diagnosed with panhypopituitarism with CDI at presentation and was treated with hydrocortisone, levothyroxine, and desmopressin. Postoperatively, she developed polyuria of more than 3L/day, with a maximum daily urine output of 7.2 L/day. Her serum sodium level decreased from 148 to 131 mEq/L. Polyuria was treated with desmopressin at incremental doses, and hyponatremia was managed with fluid replacement. At 2 months after surgery, she presented with hyponatremia-induced seizure. Polyuria and hyponatremia combined with natriuresis indicated CSWS. Treatment with fludrocortisone were initiated; then, her electrolyte level gradually normalized. CSWS is self-limiting and generally resolves within 2 weeks. However, the patient in this study still required treatment with vasopressin and fludrocortisone at 16-months after surgery. Hyponatremia in a patient with CDI may be erroneously interpreted as inadequate CDI control or syndrome of inappropriate antidiuretic hormone secretion, leading to inappropriate treatment. The identification of the potential combination of CDI and CSWS is important for early diagnosis and treatment.

• The Korean Journal of Physiology
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• v.16 no.2
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• pp.177-186
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• 1982

The effect of ethacrynic acid (EA) on the renal secretion of PAH was examined in cat kidney. $C_{PAH}$ and $T_{PAH}$ were measured before and after infusion of EA $(0.5{\sim}50mg/kg)$ through the femoral vein. The following results were obtained: 1) In the dosage range of 0.5 to 25 mg/kg, EA increased the urine flow, and sodium and potassium excretion in dose-dependent manner, but the glomelular filtration rate was decreased as the dosage of EA was increased. 2) $C_{PAH}$ and $T_{PAH}$ were decreased by EA in the dosage range of 3 to 25 mg/kg and 1 to 50 mg/kg, respectively, in dose·dependent manner with the dosage to cause 50% inhibition of about 5 mg/kg. 3) With dosage of 0.5mg/kg, EA appeared to exert a great effect on diuretic response without the influence on $T_{PAH}$. At 10min after infusion of EA, a potent diuretic effect appeared, while $T_{PAH}$ did not show a significant change. These results suggest that the action mechanism of EA on tubular secretion of PAH may be different from that on natriuresis. 4) With dosage of 5 mg/kg, EA did not inhibit the Na-K-ATPase activity in microsomal fractions from both cortex and medulla. 5) The double reciprocal plot ($l/T_{PAH}$ versus $l/P_{PAH}$) suggested that EA inhibited the P AH secretion by a competitive pattern. However, probenecid, a prototypic inhibitor of the organic acid pump, had no influence on both the inhibitory effect of $T_{PAH}$ and the natriuretic effect by EA. These results suggest that in vivo EA altered tubular secretion of P AH through interactions with receptors that are not identical with the Na-K-ATPase.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.253-261
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• 1989

Responses of atrial natriuretic peptide (ANP), aldosterone and renin release to acute volume expansion were compared in normotensive Wistar and spontaneously hypertensive rat (SHR) fed low or high-sodium diet (2 or 25 mmol Na/100 g diet). Experimental diets were fed for 6 weeks from 7-week-old and the growth rate was similar in all groups. In the morning of the experiment, catheters were inserted under ether anesthesia in femoral artery for pressure recording and blood collection, femoral vein for saline infusion, and bladder for urine collection. Then, the rats were placed in restraining cages. When the rats were recovered from anesthesia and the arterial pressure became stabilized, control urine and blood samples were collected. Then, 0.9% saline was infused for 30 min for volume expansion (3% BW). Arterial pressure was significantly higher in the high-sodium SHR but there was no difference between the two groups of Wistar rats. Control plasma levels of Na, K, ANP, renin activity, and hematocrit were not different among the 4 groups. However, plasma aldosterone level was significantly higher in the low-sodium groups. Wistar low-sodium rats showed approximately two times higher plasma aldosterone level than the SHR counterpart. Volume expansion produced a marked increase in plasma ANP level, especially in the high-sodium groups. The low-sodium groups of both strains showed approximately two-fold increase in plasma ANP level. Following a volume expansion plasma aldosterone level and renin activity decreased in all groups. There was a significant logarithmic positive correlation between plasma renin activity and aldosterone concentration. The low-sodium rats produced a greater increase in aldosterone release by small increase in plasma renin than did the high-sodium rats. The low- and high-sodium rats produced a similar degree of diuresis and natriuresis after volume expansion. However, SHR produced a greater natriuresis than did the Wistar rats. The above results indicate that regulatory mechanisms of ANP, aldosterone and renin release are different between the normotensive and hypertensive rats, and between the low- and high-sodium groups.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.103-117
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• 1982

In an effort to provide evidence as to the regulatory role of the central dopaminergic system on the renal function, the effects of centrally administered dopamine and its specific antagonist haloperidol were investigated. Haloperidol (HA) given intracerebroventricularly (i.c.v.) induced antidiuresis in doses of 15 and $50{\mu}g/kg$. With $15{\mu}g/kg$ sodium reabsorption in the tubules was increased, while with $50{\mu}g/kg$ free-water reabsorption was increased. However, a marked diuresis with increased sodium and potassium was observed with $150{\mu}g/kg$. Hemodynamic changes were not evident, indicating that the diuresis is of tubular origin. Dopamine (DA), on the other hand, produced antidiuresis when given i.c.v. in a dose-related fashion. With smaller doses of 5 and $15{\mu}g/kg$ the antidiuresis was related to increased reabsorption of sodium in the tubules, but higher doses of 50 and $150{\mu}g/kg$ the decreases in renal blood flow and glomerular filtration rate were evident in addition to the tubular action. After pretreatment with $150{\mu}g/kg$ HA, the effects of $15{\mu}g/kg$ DA was abolished, but the antidiuretic actions of 50 and $150{\mu}g/kg$ were not blocked, and the natriuretic diuretic action of HA was overcome and became inconspicuous. These observations indicate that the central dopaminergic system influences the renal function by producing antidiuresis, and HA elicits diuresis and natriuresis by competitively antagonizing DA specifically on the central dopaminegic receptors. The antidiuresis observed with smaller doses of HA can be best explained by the facts that there are more than two types of DA-receptors in the brain and that the presynaptic autoreceptors on the dopaminergic neurones which affect the dopamine release at the synapse are more sensitive than the postsynaptic receptors. Overall, these data provide an evidence indicating that the central dopaminergic system plays a role in the regulation of renal function in the rabbit.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.319-329
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• 1990

Effects of atrial natriuretic peptide (ANP) on blood pressure, plasma lenin activity, aldosterone and renal excretion were compared in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar rats fed low, medium or high sodium diet (2, 10, 25 mmol NaCl/100g diet) for 6 weeks. ANP infusion (380 ng/kg/min for 20 min) produced reductions in blood pressure, plasma renin activity, and aldosterone level, but marked increases in hematocrit, urine flow, and excretions of sodium and potassium. The low sodium group showed a significantly enhanced aldosterone lowering effect of ANP than the high sodium group. However, three salt groups showed no difference in effects of ANP on blood pressure, plasma renin activity, hematocrit and diuresis. Natriuretic response to ANP was significantly greater in the high salt-than in the low sait-SHR, but was not different between the Wistar salt groups. There were strain differences in effects of ANP: SHR showed greater responses of blood pressure and natriuresis than Wistar rats. Above results indicate that aldosterone-lowering and natriuretic effects of ANP were modifed by different dietary sodium intakes. However, blood pressure- and renin-lowering, or diuretic effects of ANP were not affected by dietary sodium intakes. The mechanisms whereby dietary sodium intakes alter the effects of ANP in the pathogenesis of hypertension are not clear.

• The Korean Journal of Pharmacology
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• v.22 no.2
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• pp.79-87
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• 1986

Recently it has been shown that central dopaminergic system regulates the renal function and that intracerebroventricularly (icv) administered dopamine (DA) produces antidiuresis and antinaturiuresis, resembling icv norepinephrine, and evidence has been accumulated which would suggest the involvement of adrenergic system in the DA effects. It was attempted therefore in this study to see whether the DA effect is influenced by pretreatment of yohimbine which is known as a specific ${\alpha}_2-adrenoceptor$ antagonist. Yohimbine produced, when given icv in doses of $100\;{\mu}g/kg$, marked antidiuresis and antinatriuresis along with decreases in renal perfusion and glomerular filtration. DA, in doses of $15\;{\mu}g/kg$, also produced antidiuresis and antinaturiuresis. However, after yohimbine-pretreatment DA $15\;{\mu}g/kg$ improved renal hemodynamics, and electrolyte excretion and urine flow rate transiently increased. With $150\;{\mu}g/kg$ DA, the antidiuresis was more marked in the control group. But the yohimbine-pretreated animals responded with marked diuresis and natriuresis, sodium excretion increasing more than three-fold, which lasted for 20 minutes. $K^+-excretion$, osmolar clearance as well as free-water reabsorption increased. Renal hemodynamics improved partly. Apomorphine, a DA agonist, when given icv in doses of $150\;{\mu}g/kg$, produced diuresis and naturiuresis, concomitant with increased renal hemodynamics. Yohimbine-pretreatment however did not abolish the apomorphine-induced diuresis and naturiuresis. Antidiuresis and antinatriuresis elicited by norepinephrine, $10\;{\mu}g/kg$, was not affected by yohimbine-pretreatment. These results indicate that the renal effects of icv DA is not so simple as those of norepinephrine, and the diuretic natriuretic cffect which had been masked by the hemodynamic effect becomes manifest only when the decreases in hemodynamics were removed by the pretreatment of yohimbine. It was further suggested that those DA receptors which mediate the natriuretic response to icv DA is not affected by yohimbine, whereas those receptors involved in the decrease in renal hemodvnamics are blocked by yohimbine. And the possibility of involvement of adrcnergic system in the DA action is not substantiated.