• YAKHAK HOEJI
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• v.43 no.5
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• pp.665-673
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• 1999

This study was performed in order to investigate the effect of ketanserin, a specific antagonist of 5-HT2 receptor, on renal function in dogs. Ketanserin (50.0 and $150.0{\;}\mu\textrm{g}/kg$), when given intravenously, produced antidiuretic action accompanied with the decreased amounts of sodium and potassium excreted in urine (ENa, EK) and the increased reabsorption rates of sodium and potassium in renal tubules (RNa, RK). Ketanserin (50.0 and $50.0{\;}\mu\textrm{g}/kg$), when administered into a renal artery, elicited antidiuretic action in both experimental and control kidney, this time changes of renal function showed the same aspect as when given intravenously. Ketanserin (15.0 and $50.0{\;}\mu\textrm{g}/kg$) injected into the carotid artery exhibited also antidiuretic action and this antidiuretic action was not affected by renal denervation. Above results suggest that ketanserin elicits antidiuretic through central function, this central antidiuretic action is not mediated by renal nerves.

• Biomolecules & Therapeutics
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• v.2 no.3
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• pp.229-235
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• 1994

In dogs, renal denervation did not affect the diuretic action accompanied with renal hemodynamic chanties and inhibition of electrolytes reabsorption rates in renal tubules by methoxyverapamil infused into the vein or into a renal artery, while renal denervation blocked the antidiuretic action due to the decreased free water and osmolar clearances along with the reduced sodium amounts excreted in urine by methoxyverpamil infused into the carotid artery. These experimental results suggest that methoxyverapamil may cause diuresis by direct action in kidney but the antidiuretic action through central function mediated by renal nerves.

• Biomolecules & Therapeutics
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• v.6 no.3
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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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• v.1 no.1
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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.

• YAKHAK HOEJI
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• v.39 no.3
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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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• v.4 no.1
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• pp.7-18
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• 1996

5-Hydroxytryptamine(5-HT, serotonin), when given into the vein, produced antidiuretic action accompanied with reduction of glomerular filtration(GFR), renal plasma flow(RPF), osmolar clearance(Cosm) and amounts of sodium or potassium excreted in urine( $E_{Na}$ , $E_{K}$), with the augmented reabsorption rates of sodium and potassium in renal tubules. 5-HT, when infused into a renal artery, exhibited diuretic action accompanied with the augmented RPF and increased $E_{Na}$ and $E_{K}$ in only infused kidney. Antidiuretic action of 5-HT infused into the vein was not influenced by ketanserin, 5-H $T_2$receptor blockade, given into a renal artery, vein or carotid artery, by methysergide, 5-H $T_1$receptor blockade, given into a renal artery, whereas above antidiuretic action was inhibited by methysergide given into vein or carotid artery. Diuretic action of 5-HT infused into a renal artery in only experimental kidney was blocked by ketanserin injected into a renal artery, was not influenced by methysergide administered into a renal artery. Above results suggest that 5-hydroxytryptamine(5-HT) produced the antidiuretic action through central 5-H $T_1$receptor and the diuretic action through 5-H $T_2$receptor located in renal tubules of kidney.ney.

• YAKHAK HOEJI
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• v.37 no.6
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• pp.561-570
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• 1993

Renal action of domperidone known as dopamine receptor blocker and effect of domperidone on renal function of dopamine were investigated in dog. Domperidone, when administered into vein, produced diuretic action by the improvement of renal hemodynamic state, when given into a renal artery, elicited diuretic action accompanied with natriuresis in only experimental kidney, whereas domperidone given into carotid artery exhibited antidiuretic action by the decrease of Na$^{+}$ excretion in urine. Diuretic action of dopamine was not influenced by domperidone given into vein or into a renal artery, was blocked by domperidone given into carotid artery. Above results suggest that domperidone produced both peripheral diuretic and central antidiuretic action, and domperidone do not block diuretic action by renal hemodynamic improvement of dopamine in kidney.

• YAKHAK HOEJI
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• v.27 no.4
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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.

• YAKHAK HOEJI
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• v.45 no.4
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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.

• YAKHAK HOEJI
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• v.38 no.5
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• pp.568-578
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• 1994

This study was performed in order to investigate the effect of diltiazem, which is a $Ca^{2+}$ channel blocker of benzothiazepine derivatives, on renal function in the dog. Diltiazem, when infused into the vein or carotid artery, produced the antidiuresis accompanied with the decreased excretion rates of sodium and potassium in urine$(E_{Na},\;E_K)$ and the increased reabsorption rates of sodium and potassium in renal tubules$(R_{Na},\;R_K)$. Diltiazem, when infused into a renal artery, exhibited the diuresis along with the increased renal plasma flow(RPF), osmolar clearance$(C_{osm})$, $E_{Na}$ and $E_K$, and decreased $R_{Na}$ and $R_K$ in only infused kidney. Above results suggest that diltiazem possess both antidiuretic action through central action and diuretic action by direct inhibition of electrolytes reabsorption rates in renal tubules, mainly distal tubule.