Stop-flow method에 依한 Ethacrynic acid의 利尿作用의 分析

鞠永棕 全南大醫大 1965 전남의대학술지 Vol.2 No.1

개의 腎臟機能에 미치는 側腦室內 Prostaglandin A₂의 影響

高光厚,鞠永棕 全南大醫大 1979 전남의대학술지 Vol.16 No.2

Role of Kappa Opioid Receptors in Central Regulation of Renal Function

Kook, Young Johng,Kim, Kyoung Sim,Lim, Young Chai,Koh, Jeong Tae,Kim, Kyung Keun Chonnam National UniversityResearch Institute of 1992 Chonnam journal of medical sciences Vol.5 No.2

Effects of Intracerebroventricular PPHT, a D_(2)-agonist, on Rabbit Renal Function

Kook, Young Johng,Jeong, Eun Taik,Kim, Kyung Keun,Lim, Young Chai Chonnam National UniversityResearch Institute of 1991 Chonnam journal of medical sciences Vol.4 No.2

Studies on Tryptaminergic Regulation of Rabbit Renal Function

Kook, Young Johng,Kim, Kyung Keun,Min, Jang Sik,Lim, Young Chai,Kook, Hoon Chonnam National UniversityResearch Institute of 1988 Chonnam journal of medical sciences Vol.1 No.2

Role of Central 5-HT_(3) Receptors in Regulation of Rabbit Renal function

Kook, Young Johng,Lim, Young Chai,Kim, Kyung Keun,Kook, Hoon,Oh, Byung Chan Chonnam National UniversityResearch Institute of 1991 Chonnam journal of medical sciences Vol.4 No.1

가토신장기능에 미치는 뇌실내 Ketanserin의 영향

국영종(Young Johng Kook),김경근(Kyung Keun Kim),임영채(Young Chai Lim),김유남(Yoo Nam Kim),국훈(Hoon Kook) 대한약리학회 1990 대한약리학잡지 Vol.26 No.2

5-Hydroxytryptamine(5-HT)를 가토뇌실내로 투여 (icv)하면 이뇨와 Na배설증가가 초래되며, 이러한 작용은 5-HT₁ 수용체길항제인 methysergide에 의하여 차단되므로 중추성 신장기능조절에 있어 중추 tryptamine계의 관련이 시사된 바 있다. 본 연구에서는 5-HT₂ 길항제로 알려진 ketanserin (KET)를 이용하여 5-HT₂ 수용체의 역할을 구명하고자 하였다. KET 120μg(=0.3μmoles)/kg icv는 신혈류역학에는 아무런 변동을 일으키지않으나 유의한 Na배설증가를 초래하여, 세뇨관에서의 Na 재흡수 감소가 시사되었다. 전신혈압은 약간 감소하였다. 정맥내 투여시에는 유의한 기능변동을 볼 수 없었다. 5-HT 200μg/kg icv는 경미하나 유의한 Na배설증가 및 이뇨작용을 나타냈다. 그러나 신장기능에 그다지 큰 영향을 미치지 않는 양인 40μg/kg의 KET icv후에는 5-HT의 작용이 크게 강화되어, Na배설분획이 9.3%에 달하였다. Norepinephrine, dopamine, histamine과 같은 다른 생체아민의 신장작용은 KET전처치에 의하여 영향받지 아니하였다. 본 연구는 중추 5-HT₁ 수용체와는 반대로 중추 5-HT₂ 수용체는 항이뇨 및 Na배설감소를 매개하고 있으며, 중추 tryptamine계는 신장기능을 이중적으로 조절하고 있음을 시사하였다. 5-Hydroxytryptamine (5-HT) was reported to elicit natriuresis and diuresis when given intracerebroventricularly (icv) and these effects were shown to be abolished by icv methysergide, 5-HT₁ antagonist, thus suggesting that central tryptaminergic system may also participate in the regulation of renal function. We tried in this study to elucidate the role of 5-HT₂ receptors in the central tryptaminergic regulation of renal function, observing the effects of icv ketanserin, a specific 5-HT₂ antagonist. Ketanserin (KET) icv in doses of 120μg (=0.3μmoles)/kg produced significant natriuresis without affecting renal hemodynamics, indicating that it resulted from decreased tubular Na reabsorption. Systemic blood pressure decreased slightly but significantly. When given iv, no significant effect was observed. 5-HT, 200μg/kg icv, produced mild but significant natriuresis and diuresis. However, after KET, 40μ g/kg icv, a dose which minimally affects renal function, the natriuresis and diuresis by 5-HT was greatly augmented, with the fractional excretion of filtered sodium reaching 9.3%. The renal effects of other biogenic amines administered icv, such as norepinephrine, dopamine and histamine, were not significantly affected by the KET pretreatment. These observations suggest that central tryptaminergic system influences renal function in dual ways, i.e., natriuretic and diuretic influence via 5-HT₁ receptors, whereas 5-HT₂ subtypes mediate the antinatriuretic and antidiuretic effects, and that the central tryptaminergic system plays a role in the regulation of rabbit renal function.

가토(家兎)의 신장기능(腎臟機能)에 미치는 측뇌실내(側腦室內) Prostaglandin F_2α의 영향(影響)

국영종(Young-Johng Kook),고광후(Kwang-Hoo Ko) 대한약리학회 1976 대한약리학잡지 Vol.12 No.2

The facts that PGE₂ produced diuresis in the rabbit when given into a lateral ventricle of the brain and that PGE_2α is abundantly found in the brain prompted us to investigate the effects of PGE_2α introduced directly into the ventricle on the renal function. PGE_2α given intraventriculary in doses of 10μg and 100μg 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 PGE_2α. Intravenously administered PGE_2α in doses of 30 to 100μg did not produce any significant change in renal function. Intraventricular PGE_2α had no effect on the systemic blood pressure, whereas intravenous administration brought about a transient hypotension. These observations suggest that PGE_2α 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 PGE_2α might play a roll in regulating renal function through the center.

가토에 있어서 측뇌실내 Bromocriptine의 신장작용

국영종(Young-Johng Kook),김경근(Kyung-Keun Kim),김재필(Jae-Pil Kim),김경호(Kyung-Ho Kim) 대한약리학회 1985 대한약리학잡지 Vol.21 No.1

가토 측뇌실내로 dopamine을 투여하면 항이뇨를 일으키고, 도파민 길항제 haloperidol은 소량에서는 항이뇨를, 대량에서는 이뇨와 Na 배설증가를 초래한다는 보고에 비추어, 본 연구에서는 중추를 통한 신장기능 조절에 관여하는 도파민 수용체의 역할을 구명코자, D-2 receptor agonist이고 D-1 antagonist인 bromocriptine(BRC)의 작용을 검토하였다. 측뇌실내로 BRC를 투여하면 20-600 μg/kg의 범위안에서 대략 용량에 비례하여 natriuresis와 이뇨가 나타났으나, 신혈류와 사구체 여과율은 증량에 따라 점차 감소하였다. 따라서 이뇨 및 Na 배설증가는 신세뇨관에서의 Na재흡수 감소에 의한 것임을 알수 있었다. 이러한 Na 배설증가는 200μg/kg에서 가장 현저하여 Na 배설분획은 약 10%에 달하였다. 그러나 600μg/kg 에서는 일시적인 현저한 혈압상승에 따르는 급격한 감소로 인하여 일시적 폐뇨가 선행한 다음 이뇨 작용이 나타났다. BRC의 정맥내 투여시에는 전신혈압 하강에 따르는 신혈류역학의 감소와 아울러 항이뇨가 나타났으며, 이는 측피실내로 투여한 BRC의 작용은 전신순환내로 유입되어 초래될 수도 있는 직접신장작용에 기인한것이 아니고 중추를 통한 것임을 시사하였다. Dopamine 150 μg/kg을 측뇌실내로 투여한 후에도 BRC 200 μg/kg은 작용을 나타낼 수 있으나, dopamine 500 μg/kg에 의해서는 BRC의 작용이 소실 되었다. 24 시간전에 1 mg/kg의 reserpine으로 처리한 가토에서는 200 μg/kg BRC의 작용이 오히려 더 빠르고 강화되었다. 일측신장 신경을 제거한 표본에서는, BRC투여로 대조신은 항이뇨를 나타냈으나 실험신(탈신경측)은 심한 이뇨와 Na배설 증가를 일으켰다. 이상의 실험결과는, 측뇌실내 BRC는 natriuretic factor를 유리시킴과 동시에 교감신경 긴장도를 증가시키는 것을 시사하였으며, 또한 가토 신장기능의 중추 도파민계를 통한 조절에 있어서 여러 도파민 수용체가 각각 다른 기능을 하고 있음을 시사하였다. In view of the facts that dopamine (DA) when given directly into a lateral ventricle (i.c.v.) of the rabbit brain induces antidiuresis and that haloperidol, a non-specific antagonist of DA receptors, produces anti-diuresis in smaller doses and diuresis and natriuresis in larger doses, the present study was undertaken to delineate the roles of various DA receptors involved in the center-mediated regulation of renal function. Bromocriptine (BRC), a relatively specific agonist of D-2 receptors and at the same time a D-,1 antagonist, elicited natriuresis and diuresis when given i.c.v. in doses ranging from 20 to 600 μg/kg, roughly in dose-related fashion, while the renal perfusion and glomerular filtration progressively decreased with doses, indicating that the diuretic, natriuretic action resides in the tubules, not related to the hemodynamic effects. These diuresis and natriuresis were most marked with 200 μg/kg, with the fractional sodium excretion reaching about 10%. With 600 μg/kg, however, the diuretic, natriuretic action was preceded by a transient oliguria resulting from severe reduction of renal perfusion, concomitant with marked but transient hypertension. When given intravenously, however, BRC produced antidiuresis and antinatriuresis along with decreases in renal hemodynamics associated with systemic hypotension, thus indicating that the renal effects produced by i.c.v. BRC is not caused by a direct renal effects of the agent which might have reached the systemic circulation. In experiments in which DA was given i.c.v. prior to BRC, 150 μg/kg DA did not affect the effects of BRC (200 μg/kg), while 500 μg/kg DA abolished the BRC effect. In rabbits treated with reserpine, 1 mg/kg i.v.,24 h prior to the experiment, i.c.v. BRC could unfold its renal effects not only undiminished but rather exaggerated and more promptly. In preparations in which one kidney is deprived of nervous connection, the denervated kidney responded with marked diuresis and natriuresis, whereas the innervated, control kidney exhibited antidiuresis. These observations suggest that i.c.v. BRC influences the renal function through release of some humoral natriuretic factor as well as by increasing sympathetic tone, and that various DA receptors might be involved with differential roles in the center-mediated regulation of the renal function.

측뇌실내(側腦室內) Nalprphine의 가토신장기능(家兎腎臟機能)에 미치는 영향(影響)

국영종(Young Johng Kook),최봉규(Bong Kyu Choi),김흥규(Heung Kyu Kim) 대한약리학회 1980 대한약리학잡지 Vol.16 No.2

As it has been reported that morphine induce antidiuresis, and antinatriuresis along with decrease in renal hemodynamics when given intracerebroventricularly[ivt], the renal action of nalorphine, a partial antagonist of morphine action, and its influence upon the morphine action were investigated in this study. 10μg/kg of nalorphine given into the lateral ventricle of the rabbit brain tended to decrease renal plasma flow and glomerular filtration rate and increase the reabsorption of free water in the tubules. 100μg/kg ivt significantly decreased urine flow rate and increased free water reabsorption, and tended to increase electrolyte excretion in spite of decrease in renal plasma flow and glomerular filtration, suggesting that ADH also involved in the antidiuresis. Morphine hydrochloride, 10μg/kg, ivt, produced marked decrement in renal hemodynamics along with decreased excretions of sodium, potassium and water, and these morphine actions were alleviated by nalorphine given 20 min later. The natriuretic action of ivt nalorphine manifested itself uninfluenced by the morphine. These observations indicate that nalorphine ivt produces renal actions similar to those of morphine, though less potent, and that it can antagonize the latter action. It is suggested that morphine influences renal hemodynamics through nerve by stimulating the morphine receptor in the brain, whereas nalorphine liberates ADH by the agonistic action on the nalorphine receptor .