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

• Biomolecules & Therapeutics
• /
• v.8 no.1
• /
• pp.44-52
• /
• 2000

SKP-450 which is $K^{+}$ channel opener, When given into duodenum, exhibited the decline of urine flow accompanied with the decrease of glomerular filtration rates (GFR), renal plasma flow (RPF), N $a^{+}$ and $K^{+}$ excreated in the urine ( $E_{Na}$ , $E_{K}$) and the increase of $K^{+}$N $a^{+}$ratios, and then appeared the significant fall of mean arterial pressure (MAP) and unchanged of reabsorption rates of N $a^{+}$, $K^{+}$ in renal tubules ( $R_{Na}$ , $R_{K}$). SKP- 450 injected into the vein elicited the decline of urine flow along with the reduction of $E_{Na}$ , $E_{K}$, and the increase of $R_{Na}$ , $R_{K}$ and $K^{+}$M $a^{+}$ ratios. SKP-450 administered into a renal artery produced diuretic action along with the increase of $E_{Na}$ , $E_{K}$ and the decrease of $R_{Na}$ , $R_{K}$ in experimental kidney, whereas produced the same aspect to intravenous SKP-450 in the control kidney. Above results suggest that SKP-450 possess both diuretic action in the kidney and central antidiuretic action in dog.tic action in dog.tion in dog.

• Biomolecules & Therapeutics
• /
• v.1 no.2
• /
• pp.151-159
• /
• 1993

Effect of yohimbine, a specific antagonist for presynaptic adrenoceptor, on the renal action of clonidine, a specific presynaptic adrenoceptor agonist, was investigated in dog. Clonidine, when given intravenously, produced diuretic action accompanied with augmentation of osmolar and free water clearance (Cosm and 4C_{H_2O}$), and elicited the increase of amounts of sodium and potassium excreted in urine ($E_{Na}\; and\; E_k$). These actions of clonidine were inhibited by yohimbine either injected intravenously or infused into a renal artery. Clonidine, when infused into a renal artery, produced antidiuretic action accompanied with decreased of glomerular filtration rate (GFR) and renal plasma flow (RPF), and exhibited the reduced amounts of sodium and potassium in urine. These actions of clonidine injected into a renal artery were blocked by yohimbine administered either into vein or into a renal artery. Above results suggest that yohimbine block the renal action of clonidine only in central system, do not in kidney.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1994.04a
• /
• pp.285-285
• /
• 1994

Naproxen을 개의 정맥내 투여하였을때 뇨량의 감소와 더불어 삼투질제거율(Cosm), 뇨중 $Na^{+}$과 $K^{+}$의 배설율( $E_{Na}$ , $E_{k}$ )의 감소와 신세뇨관에서의 $Na^{+}$과 $K^{+}$의 재흡수율( $R_{Na}$ , $R_{k}$ )과 K/Na비의 증대를 나타내었으며 신혈류량(RPF)이 감소하였다. 한쪽 신동맥내에 naproxen을 투여하였을때 투여신(실험신)에서의 이뇨작용과 대조신에서의 항이뇨작용을 나타내었다. 경동맥에 naproxen을 투여하였을때도 뚜렷한 항이뇨작용을 나타내었다. 이와같은 두경우에서의 항이뇨 작용시의 신기능변화는 정맥내 naproxen의 경우와 같은 양상을 나타내었다. 경동맥내의 naproxen의 항이뇨작용은 신신경 제거에 의하여 영향을 받지 않았으나 정맥내로의 arachidonic acid나 indomethacin의 전처리에 의하여서는 나타나지 않았다. 경동맥내의 naproxen은 정맥내의 spironolactone의 이뇨작용을, 정맥내의 spironolactone은 경동맥내의 naproxen의 항이뇨작용을 억제하였다. 이상의 결과로 보아 naproxen은 중추성 항이뇨작용과 $Na^{+}$저류를 나타내며 이는 prostaglasdin의 합성억제와 aldosterone양 작용에 의하는 것으로 사료된다.

• Biomolecules & Therapeutics
• /
• v.7 no.3
• /
• pp.249-256
• /
• 1999

Glibenclamide(GLY)(1.0 and 3.0 mg/kg), an ATP-dependent $K^+$ channel blocker, when given into the vein in dogs, produced the diuretic action accompanied with the increase of osmolar clearance($C_{osm}$), urinary excretion of $Na^+$ and $K^+$ ($E_{Na}$, $E_K$), and with the decrease in reabsorption rates for $Na^+$ and $K^+$ in renal tubules ($R_{Na}$, $R_K$), and then ratios of $K^+$ against $Na^+$($K^+$/$Na^+$) were decreased. GLY did not affect mean arterial pressure at any doses used. At a low dose(0.1 mg/kg), GLY injected into a renal artery brought about the diurectic action in both experimental and control kidney, however at a higher dose(0.3 mg/kg), GLY appeared significant diuretic action in the control kidney, but not in experimental kidney and the decrease of glomerular filtration rates(GFR), renal plasma flow(RPF), $E_K$, and the increase in $E_{Na}$. In the control kidney, these changes in renal function exhibited the same aspect as shown in intravenous experiments. In experiments given into carotid artery of GLY(0.5 and 1.5 mg/kg), changes in all renal function included the increase in urine volume were the same pattern as shown in intravenous experiments. The above results suggest that glibenclamide produces diuretic action through central function and the action site of the GLY in kidney is the renal distal tubules in dogs.

• YAKHAK HOEJI
• /
• v.36 no.1
• /
• pp.46-55
• /
• 1992

Methoxyverapamil, $Ca^{2+}$ channel blocker, when given intravenously by means of bolus, produced the transient increase of urine flow, and then methoxyverapamil was infused in this experiments. Methoxyverapamil, when infused into vein, elicited the increase of urine flow ancampanied with the increased glomeralar filtration rate(GFR), renal plasma flow(RPF), excretion amounts of sodium and potassium in urine($E_{Na},\;E_k$) and osmolar clearance(Cosm), wherease produced the no change of free water clearance($C_{H2O}$) and the reduction of reabsorption rates of sodium and potassium in reral tubules($R_{Na},\;R_k$). Methoxyverapamil, when infused into a renal artery, exhibited the diuretic action in only infused Kidney, at this time changes of renal function were the same aspect to that of intravenously infused methoxyverapamil. Methoxyverapamil, when infused into a carotid artery, exhibited the decreased urine flow along with the reduction of Cosm, $C_{H2O}\;and\;E_{Na}$. Above results suggest that methoxyverapamil possess both the diuretic action by direct action in kidney and antidiuretic action through the central function.

• Biomolecules & Therapeutics
• /
• v.9 no.3
• /
• pp.209-217
• /
• 2001

This study was attempted to investigate on renal effect of ($\pm$)6-chloro-7,8-dihydroxy-1-phenol 2,3,4,5-tetrahydro-lH-3 benzazepine (SKF 81297), dopamine $D_1$ receptor agonist, in dog. SKF 81297, when gluten intravenously, produced diuretic action along with the increases of renal plasma flow (RPF), glomerular filtration rate (GFR), amounts of N $a^{+}$ and $K^{+}$ excreted into urine ( $E_{Na}$ , $E_{K}$) and osmolar clearance ( $C_{osm}$). It also decreased the reabsorption rates of N $a^{+}$ and $K^{+}$ in renal tubule ( $R_{Na}$ , $R_{K}$) and free water clearance ( $C_{H2O}$), whereas ratios of $K^{+}$ agonist N $a^{+}$ in urine and filtration fraction (FF) was not changed. SKF 81297, when administered into a renal artery, elicited diuresis both in experimental kidney given the SKF 81297 and control kidney not given, while the effect was more remarkable in experimental kidney than those exhibited in control kidney. SKF 81297 given into carotid artery also exhibited diuresis, the potency at this time, compared to those induced by intravenous SKF 81297, was magnusgreat. Above results suggest that SKF 81297 produces diuresis by both indirect action through changes of central function and direct action being induced in kidney. Central diuretic action is mediated by improvement of renal hemodynamics, but direct action by inhibition of electrolytes reabsorption in renal tubule.enal tubule. tubule.

• YAKHAK HOEJI
• /
• v.45 no.2
• /
• pp.205-213
• /
• 2001

The dopaminergic receptors were consisted of two distinct subtypes, $D_1$and $D_2$, each having different function. The present study was attempted to investigate the effects of R(-)-2,10,11-trihydroxy-N-n-propylnoraporphine (TNPA), a dopamine $D_2$receptor agonist, on renal function in dog. TNPA (5.0~15.0 $\mu$g/kg), when given into the vein, produced a dose-dependently antidiuresis along with the decrease in osmolar clearance ( $C_{osm}$) and urinary excretion of sodium and potassium ( $E_{Na}$ , and $E_{K}$). It also increased reabsorption rates of sodium and potassium in renal tubules ( $R_{Na}$ , $R_{K}$) without any changes in glomerular filtration rate (GFR), renal plasma flow (RPF) and free water clearance ( $C_{H2o}$). TNPA (0.5~1.5 $\mu$g/kg/min) infused into a renal artery decreased urine flow both in the experimental and the control kidneys. TNPA (1.5~5.0 $\mu$g/kg) administered via the carotid artery also greatly exhibited antidiuresis even at intravenously ineffective doses. Changes of renal function by TNPA given into both the renal artery and the carotid artery were almost the same aspect to those induced by intravenous TNPA. These results obtained from the present study suggest that TNPA produces antidiuresis by increasing the reabsorption rates of electrolytes in renal tubules, mainly distal tubule, through changing of central function.unction.

• YAKHAK HOEJI
• /
• v.40 no.4
• /
• pp.468-477
• /
• 1996

Vasopressin which is an antidiuretic hormone in human body produced the diuretic action in dog. This study was investigated in order to certify the diuretic action and to search out the mechanism of the action on the vasopressin. Vasopressin, when given in a dose of 10.0mU/kg, bolus+1.0mU/kg/min intravenously, exhibited the increase of urine flow(Vol), renal plasma flow(RPF), osmolar clearance (Cosm) and amounts of sodium and potassium excreted in urine ($E_{Na},\;E_K$), the decrease of reabsorption rate of sodium and potassium in renal tubules ($R_{Na},\;R_K$), and then elevated the mean arterial pressure(MAP). Vasopressin given in a increased dose to 30.0mU/kg, bolus+1.0mU/kg/min intravenously elicited the same aspect with that exhibited by a small dose in changes of Vol. and all renal function and potentiated the change rates, whereas this time MAP did not change at all when compared with control value. Vasopressin, when administered into a renal artery, did not induce the changes of Vol and all renal function in experimental (administered) kidney, but increased slightly the Vol, glomerular filtration rate(GFR), $E_{Na},\;and\;E_K$ expected the no change of $R_{Na}\;and\;R_K$ in the control (not administered) kidney. Vasopressin, when infused into carotid artery, showed the increase of Vol. GFR, $E_{Na},\;and\;E_K$ and no change of $R_{Na}\;and\;R_K$ in a dose of 1/5 of intravenous dose. Diuretic action of vasopressin administered into carotid artery was not influenced by renal denervation. Above results suggest that vasopressin produced diuretic action by hemodynamic changes in dogs. These hemodynamic changes may be mediated by central endogenous substances not associated with renal nerve.

• YAKHAK HOEJI
• /
• v.33 no.3
• /
• pp.183-190
• /
• 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.