• Biomolecules & Therapeutics
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• 제3권2호
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• pp.136-142
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• 1995

This study was performed in order to certify the antidiuretic action and to investigate the mechanism of antidiuretic action of debrisoquin infused into a renal artery in dog. Debrisoquin, when infused into a renal artery, exhibited the antidiuretic action accompanied the reductions of glomerular filtration rate and renal plasma flow, and the decreased amounts of sodium and potassium excreted in urine, limited only to the infused side, while control kidney function remained unchanged at all. The antidiuretic action of debrisoquin infused into a renal artery was blocked by pretreament of prazosin, $\alpha$$_1$-adrenergic blocking agent, or reserpine, catecholamine depleting agent. These results suggest that debrisoquin infused into a renal artery elicits antidiuretic action through indirect stimulation of renal sympathetic nerves.

• 약학회지
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• 제39권3호
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• pp.314-328
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• 1995

This study was attempted to investigate the mechanism of retention of sodium and water by naproxen which is a drug among nonsteroidal anti-inflammatory drugs in dogs. Napoxen, when given intravenously in doses ranging from 30 mg to 100 mg/kg, elicited antidiuresis accompanied vath the decrease of osmolar clearance(Cosm) and amounts of sodium excreted in urine(E$_{Na}$), with the increase of sodium reabsorption rate in renal tubule(R$_{Na}$) and ratio of potassium against sodium (K/Na). Naproxen infused into a renal artery in doses ranging from 1.0mg to 3.0mg/kg/min produced both diuretic action in infused kidney and antidiuretic action in control kidney. Naproxen injected into carotid artery in doses ranging from 10.0 mg to 30.0 mg/kg exhibited antidiuretic action. Changes of renal function in the circumstances of above two antidiuresis were the same with aspect of intravenous naproxen. Antidiuretic action of naproxen injected into carotid artery was not affected by renal denervation, was blocked by pretreatment with i.v. arachidonic acid, prostaglandin precursor, or i.v. indomethacin, cyclooxygenase inhibitor. Naproxen injected into carotid artery abolished the diuretic action of i.v. spironolactone, aldosterone antagonist, and i.v. spironolactone blocked the antidiuretic action of naproxen given into carotid artery. The results suggest that naproxen produced antidiuresis, and sodium and water retention through the central system, the mechanism being related to the prostaglandin biosynthetic inhibition and aldostercfne like action.

• Biomolecules & Therapeutics
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• 제6권3호
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• pp.225-231
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• 1998

This studies were performed for investigation of mechanism on central antidiuretic action of L$_{G}$-Nitro-L-arginine (L-NOARG), nitic oxide systhase inhibitor, in dog. Antidiuretic action of L-NOARG infused into the carotid artery was not affected by renal denervation but inhibited by pretreatment with arginine, NO Precusor. Furthermore, L-NOARG inhibited the diuretic action of dopamine induced by hemodynamic development. Above results suggest that antidiuretic actions of L-NOARG mediated by endogenous substances not associated with renal nerve. Therefore, it is demonstrated that those endogenous substances might be associated with NO which mediate the diuretic action of dopamine.e.

• Biomolecules & Therapeutics
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• 제8권2호
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• pp.125-131
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• 2000

Idazoxan, $\alpha$$_2$-adrenergic antagonist, produced antidiuretic action by administration into the vein and diuretic action only in ipsilateral kidney by injection into a renal artery in dog. These studies were performed for investigation of mechanism on the renal action induced by idazoxan. Antiduretic action by idazoxan given into vein and diuretic action only in ipsilateral kidney by idazoxan injected into a renal artery were blocked entirely by renal denervation. Antidiuretic action of idazoxan given into the vein was weakened by UK 14,304, $\alpha$$_2$-adrenergic agonist, pretreated into the vein. Above results suggest that antidiuretic action of idazoxan given into the vein is caused by blocking of $\alpha$$_2$-adrenergic receptor, diuretic action only in ipsilateral kidney of idazoxan injected into a renal artery by blocking of $\alpha$$_2$-adrenergic receptor in the kidney.

• Biomolecules & Therapeutics
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• 제1권1호
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• pp.84-92
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• 1993

This study was performed to elucidate the mechanism of antidiuretic action of diltiazem by infusion into the vein and carotid artery, of diuretic action into a renal artery in dog. Renal denervation caused a reversal of the effect of diltiazem from the antidiuretic to the diuretic when infused into vein or carotid artery, and potentiated the diuretic effect when infused into a renal artery. The changes of renal function in diuretic circumstances as described above included the increase in renal plasma flow, osmolar clearance, the amounts of sodium and potassium excreted in urine and the decrease in reabosrption rate of sodium and potassium in renal tubules. Above results suggest that antidiuretic action of diltiazem may be mediated by central nervous system, not by endogenous substance, diuretic action by direct renal action.

• 약학회지
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• 제45권4호
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• pp.397-406
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• 2001

It has been demonstrated previously that R(-)-2,10,11-trihydroxy-N-n-propylnora porphine (TNPA), a dopamine D$_2$receptor agonist, produced the antidiuresis through changes of central friction in dog. This study was investigated about effects of renal denervation and raclopride, a dopamine D$_2$receptor antagonist, on the antidiuresis of TNPA in order to elicidate the mechanism involved in this central antidiuresis induced by TNPA. Antidiresis exhibited by TNPA given into the vein or into carotid artery was not influenced by renal denervation, whereas antidiuresis of TNPA administered into carotid artery was blocked almost perfectly by raclopride pretreated into carotid artery. From these observations it is concluded that central antidiuresis induced by TNPA is brought about through activation of dopamine D$_2$receptor localized in brain, not related to renal nerve activity.

• 약학회지
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• 제27권4호
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• pp.271-282
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• 1983

This study is an attempt to study the influence of clonidine, which has a central sympatholytic action, on the renal function in dogs and to elucidate its mechanism of action. Clonidine ($15\mu$g/kg) injected into a cephalic vein of the dog produced a marked increase in urine flow and in amounts of $Na^{+}$ and $K^{+}$ excreted in urine, and clearances of free water and osmolar substance, the reabsorption rates of $Na^{+}$ and $K^{+}$ in renal tubules were significantly decreased. Clonidine ($50.0]mu$g/kg) administered intravenouly elicited a transient reduction in urine flow, along with inhibition of all renal functions. Intravenous clonidine-induced diuretic effect was completely blocked by pretreatment with reserpine, and was lessened by water diuresis. Clonidine ($3.0\mu$g/kg) injected tnto a carotid artery revealed a transient diuresis with a increase in clearance of free water. Clonidine injected into a renal artery showed a significant antidiuretic effect and all functions of an experimental kidney were reduced. Antidiuretic action induced by clonidine given into a renal artery markedly suppressed by pretreatment with reserpine. The above results suggest that clonidine has dual mechanisms: 1) diuretic effect due to the central sympatholytic action and inhibition of release of antidiuretic hormone, and 2) antidiutetic effect indued by indirect symptheic stimulation in the periphery.

• 약학회지
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• 제33권3호
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• pp.183-190
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• 1989

Angiotensin II, adminstered (infused or injected) intravenously, elicited the antidiuretic action with the decreased parameters of renal function at a small dose ($0.01\;{\mu}g/kg/min$), whereas, at a large dose (0.03, $0.1\;{\mu}g/kg/min$ and $5.0\;{\mu}g/kg$), it produced the diuretic action accompanied the increased amounts of sodium and potassium excreted in urine ($E_{Na}\;and\;R_K$). At this time, glomerular filtration rates (GFR) were weakened slightly and renal plasma flows (RPF) were reduced markedly, and then filtration fractions (FF) were increased. Angiotensin II, infused into a renal artery, exhibited antidiuretic action at a small dose ($0.003\;{\mu}g/kg/min$), and diuretic action at a large dose ($0.01\;{\mu}g/kg/min$), only in infused (experimental) kidney. The mechanism of the action was similar to the cases of the intravenous angiotensin II. The above results suggest that angiotensin II of a large dose produced diuretic action due to mechanism inhibiting reabsorption of electrolytes in renal tubules, mainly in proximal tubule in dog.

• Clinical and Experimental Pediatrics
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• 제50권5호
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• pp.430-435
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• 2007

Even though we drink and excrete water without recognition, the amount and the composition of body fluid remain constant everyday. Maintenance of a normal osmolality is under the control of water balance which is regulated by vasopressin despite sodium concentration is the dominant determinant of plasma osmolality. The increased plasma osmolality (hypernatremia) can be normalized by the concentration of urine, which is the other way of gaining free water than drinking water, while the low plasma osmolality (hyponatremia) can be normalized by the dilution of urine which is the only regulated way of free water excretion. On the other hand, volume status depends on the control of sodium balance which is regulated mainly by renin-angiotensin-aldosterone system, through which volume depletion can be restored by enhancing sodium retention and concomitant water reabsorption. This review focuses on the urine concentration and dilution mechanism mediated by vasopressin and the associated disorders; diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion.

• Journal of Pharmaceutical Investigation
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• 제14권2호
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• pp.92-103
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• 1984

The action of debrisoquine on renal function in rabbits was studied. 1. When debrisoquine was given into ear vein, it did not affect on renal functin with smaller doses of 0.1 or 0.3mg/kg, while with higher dose of 1.0mg/kg it elicited the significant decrease of urine flow, renal plasma flow and glomerular filtration rate, and the increase of filtration fraction, and at the same time sodium excreted in urine, FENa (fractional excretion of sodium) and osmolar clearance were significantly decreased, and then it exhibited the increase of $K^+/Na^+$ ratio and no changes of $T^cH_2O$. 2. Debrisoquine (1.0mg/kg), when injected repeatedly into a vein, produced a more marked decrease of urine flow. 3. Debrisoquine induced-antidiuretic action was not affected by pretreatment with phentolamine (2mg/kg, i.v.), alpha-sympathetic blocking agent. 4. Debrisoquine given intracerebroventricularly did not produce a significant change on renal function in dose of 0.1mg/kg. These results suggest that debrisoquine produce the antidiuretic effect in rabbit, and the mechanism of its action is due to dual actions that are the decrease of hemodynamic effect and the facilitation of reabsorption of sodium in renal tubules.