• The Korean Journal of Physiology
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• v.23 no.2
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• pp.377-391
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• 1989

Recently it was suggested that the endogenous adenosine might be the mediator for the intercellular communication in the regulation of tubuloglomerular feedback control and renin release. Even though the previous data showed more important regulatory roles in the renal hemodynamics and renin release for the A1 adenosine receptor, it has not yet been settled down about the functional subclassification of renal adenosine receptors. The purpose of the present experiment was to clarify the importance of the renal adenosine receptors for the regulations of the hemodynamic, excretory and secretory functions. Experiments have been done in unanesthetized rabbits. Intrarenal arterial infusion of A1 adenosine antagonist, 8-phenyltheophylline, $3{\sim}30\;nmole/min$, increased urine flow, renal hemodynamics and urinary excretion of sodium. Intrarenal arterial infusion of Al antagonist, 1-3-diethyl-8-phenylxanthine (DPX), $10{\sim}100\;nmole/min$, increased renal hemodynamics and excretory functions. Non-specific adenosine antagonist, theophylline, $30{\sim}300\;nmole/min$, resulted in dose dependent increases in renal hemodynamics and excretory function. All of the three adenosine antagonists for the increases in renal hemodynamics, excretory and secretory functions was 8-phenyltheophylline > DPX > theophylline. These results suggest that the endogenous adenosine is important for the intrinsic regulatory roles for the renal functions through the adenosine receptors, and that the A1 adenosine receptor is more important than the A2 receptor in the regulation of renal hemodynamics, excretory and renin secretory functions.

• The Korean Journal of Pharmacology
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• v.16 no.1 s.26
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• pp.15-24
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• 1980

As it has been reported that opioids such as morphine and methionine-enkephalin induced antidiuresis and antinatriuresis along with decrease in renal hemodynamics when given intracerebroventricularly(ivt), the renal action of ivt naloxone, a pure antagonist of morphine, and its influence upon the morphine action were investigated in this study. Less than $0.3{\mu}M/kg$ naloxone ivt did not change renal funtion. $1{\mu}M/kg$ ivt tended to, increase urine flow rate and induce transient natriuresis. $3{\mu}M/kg$ ivt produced transient: natriuresis. $3{\mu}M/kg$ ivt produced marked diuresis and natriuresis without any changes of renal hemodynamics. $10{\mu}M/kg$ ivt produced significant increases of urine flow rate and excretion of sodium without any changes of renal hemodynamics. Morphine $0.03{\mu}M/kg$ ivt produced marked decrement in renal hemodynamics along with decreases of water and sodium excretion, as previously shown by Kang. These effects of ivt morphine were completely abolished by the pretreatment with $0.3{\mu}M/kg$ naloxone. These observations provide further evidence that opiate receptors and endorphins in the brain might play an important role in the center-mediated regulation of the renal function in the rabbit.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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• pp.1-7
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• 1980

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. $10{\mu}g/kg$ 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. $100{\mu}g/kg$ 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, $10{\mu}g/kg$, 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'.

• The Korean Journal of Physiology
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• v.19 no.1
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• pp.35-48
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• 1985

One of most frequently used anesthetic agents is barbiturate derivatives. Pentobarbital or thiopental sodium have been used most frequently in the laboratory or clinical practice. There have been reports on the renal effects of barbiturate anesthesia in human and laboartory animals. Renal effects of thiopental sodium anesthesia, however, are still controversial. One of the discrepancies may be derived from the doses used. It has been reported that subanesthetic small dose of thiopental sodium influences the renal function directly. To clarify possible central effects of very small amounts of thiopental sodium on the renal function, experiments have been done in conscious rabbits. Thiopental sodium was infused into the lateral cerebroventricle for 10 minutes. Intracerebroventricular thiopental sodium induced increased urinary volume, glomerular filtration rate and renal plasma flow by doses of $0.1{\sim}1.0\;mg/10 min/rabbit$. Filtration fractions were not changed. Sodium, chloride and potassium excretions were increased by 0.065 mg/10 min/rabbit of thiopental sodium without significant changes of renal hemodynamics. Higher doses of thiopental sodium $(0.1{\sim}1.0\;mg/10 min/rabbit)$ induced greater increases of electrolytes excretion and renal hemodynamics. Free water clearance was not changed by thiopental sodium, but the fractional excretion of free water showed a tendency of decrease. Fractional excretion of sodium was increased by doses of 0.065 to 1.0 mg of thiopental sodium . Highly significant correlation between the changes of glomerular filtration rate and the changes of sodium excretion were found in the higher doses. Plasma renin concentration (activity) was not changed by the centrally administered thiopental sodium. Intravenous thiopental sodium, 1.0 mg/rabbit, induced no changes of renal function in conscious rabbit. These data suggest that intracerebroyentricular thiopental sodium can increase urinary sodium excretion directly by inhibition of sodium reabsorption in the renal tubules and/or indirectly by increasing the renal hemodynamics.

• Toxicological Research
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• v.17
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• pp.117-125
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• 2001

Envenoming by Russells viper causes a broad spectrum of renal impairment. Renal failure is an important complication in patients bitten by Russells viper. Experimental work in animals and in vitro has elucidated pathophysiological mechanisms that contribute to life threatening complications and have suggested possibilities for therapeutic intervention. The evidence in experimental animals regarding mechanisms of venom action in relation to changes in either extrarenal or intrarenal factors is presented. The cardiovascular system and renal hemodynamics are affected by venom. Reductions of renal function including renal hemodynamics are associated directly with changes in general circulation during envenomation. Possible endogenous mechanisms for releasing the hormone inducing renal vasoconstriction after envenomation are evident. Hormonal factor such as the catecholamine, prostaglandin and renin angiotensin systems induce these changes. Direct nephrotoxicity of venom action is studied in the isolated per-fused kidney. Characteristic polarization of the cell membrane, changes of mitochondrial activity and Na-K ATPase in renal tubular cells are observed. Changes in renal function and the cardiovascular system are observed of ter envenomation and are reversed by the administration of Russells viper antivenom (purified equine immunoglobulin, $Fab_2$ fragment). The neutralizing effects are more efficient when the intravenous injection of antivenom is given within 30 min after the envenomation.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.555-563
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• 1998

The renal function is under regulatory influence of central nervous system (CNS), in which various neurotransmitter and neuromodulator systems take part. However, a possible role of central GABA-benzodiazepine system on the central regulation of renal function has not been explored. This study was undertaken to delineate the renal effects of diazepam. Diazepam, a benzodiazepine agonist, administered into a lateral ventricle (icv) of the rabbit brain in doses ranging from 10 to 100 ${\mu}g/kg,$ elicited dose-related diuresis and natriuresis along with improved renal hemodynamics. However, when given intravenously, 100 ${\mu}g/kg$ diazepam did not produce any significant changes in all parameters of renal function and systemic blood pressure. Diazepam, 100 ${\mu}g/kg$ icv, transiently decreased the renal nerve activity (RNA), which recovered after 3 min. The plasma level of atrial natriuretic peptide (ANP) increased 7-fold, the peak coinciding with the natriuresis and diuresis. Muscimol, a GABAergic agonist, 1.0 ${\mu}g/kg$ given icv, elicited marked antidiuresis and antinatriuresis, accompanied by decreases in systemic blood pressure and renal hemodynamics. When icv 0.3 ${\mu}g/kg$ muscimol was given 3 min prior to 30 ${\mu}g/kg$ of diazepam icv, urinary flow and Na excretion rates did not change significantly, while systemic hypotension was produced. These results indicate that icv diazepam may bring about natriuresis and diuresis by influencing the central regulation of renal function, and that the renal effects are related to the increased plasma ANP levels, not to the decreased renal nerve activity, and suggest that the effects may not be mediated by the activation of central GABAergic system.

• The Korean Journal of Physiology
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• v.20 no.1
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• pp.103-124
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• 1986

Since it has been suggested that atrial receptor may be involved in the mechanism of extracellular volume regulation, it was shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of cardiac atrial tissue, when injected intravenously into anesthetized rats, was shown to cause a large and rapid increase in renal excretion of sodium. Various natriuretic peptides were isolated and synthetized, and the effects were investigated by many workers. Most studies, however, have been carried out under anesthesia and there have teen some controversies over direct effect of the factor on the renal function. Therefore, it was attempted in this study to access the effects of an atrial extract and a synthetic natriuretic factor in unanesthetized rabbits. Intrarenal arterial infusion of atrial extract caused a rapid increase of urinary volume and excretion of sodium. Glomerular filtration rate and renal plasma flow were both increased with no change in filtration fraction. The ventricular extract produced no change in urinary excretion of electrolytes, nor in renal hemodynamics. Intrarenal infusion of synthetic atrial natriuretic factor caused increases of renal excretory rate of sodium, chloride and potassium, and $FE_{Na}$. Glomerular filtration rate, renal plasma flow increased. And free water clearance also increased. Accentuated excretory function correlated well with increased glomerular filtration rate and renal plasma flow during infusion and for 10 minutes following the cessation of the infusion. Renin secretion rate decreased during constant infusion of atrial natriuretic factor. However, no correlation was found with the changes in glomerular filtration rate, renal plasma flow, or urinary excretion of sodium. These results suggest that atrial extract or atrial natriuretic factor induces changes in renal hemodynamics, as in excretion of electrolytes either indirectly through hemodynamic changes or directly by inhibiting tubular reabsorption. At the same time, renin secretory function is affected by the factor possibly through an unknown mechanism.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.413-419
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• 2001

This study was performed to evaluate the renal hemodynamics using color Doppler ultrasonography in dogs with unilateral experimental hydronephrosis treated with transarterial embolization of the renal artery (TAE-RA). Experimental hydronephrosis was induced by ligation of unilateral ureter in 12 dogs. The mean resistive index (RI) value of kidney was significantly increased at 4, 9, 17 days after ligation of ureter. Unilateral hydronephrosis was established in 12 dogs at 17 days after ligation of ureter. Renal artery embolization was performed using selective catheterization in the hydronephrotic kidney of seven dogs and EKG, $SpO_2$body temperature, pulse, and respiratory rate were within normal ranges during procedures. There were no dogs expired after TAE-RA and no side effects associated with regurgitation of iohexol-ethanol solution. In color Doppler ultrasonographic findings, there was no blood flow into the embolized kidneys treated by TAE-RA, however, blood flow signal was found in contralateral normal kidney of dogs treated with TAE-RA compared to that of normal kidney in normal control group. It is concluded that TAE-RA does not affect the hemodynamics of contralateral normal kidney in dogs with experimental hydronephrosis and color Doppler ultrasonography is simple and non-invasive modality for the monitoring of the revascularization of the renal artery after TAE-RA.

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.3
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• pp.215-217
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• 2017

Branchio-oto-renal syndrome (BOR) is a rare autosomal dominant disorder. The features include branchial cysts, hearing loss, ear malformation, preauricular pits, retrognathia, congenital heart disease, and renal abnormalities. However, anesthetic management of these patients has seldom been reported. We report a case in which general anesthesia was performed for dental treatment in a patient with BOR. Airway management, renal function, and hemodynamic changes can be of critical concern during anesthetic management. A 13-year-old girl diagnosed with BOR had severe right hearing loss, right external ear malformation, renal abnormalities, and postoperative patent ductus arteriosus (PDA). Dental extraction under general anesthesia was scheduled for a supernumerary tooth. The procedure was completed with sufficient urine volume, adequate airway management, and stable hemodynamics.

• The Korean Journal of Pharmacology
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• v.16 no.1 s.26
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• pp.51-56
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• 1980

Phytolaccae Radix (PR), Brunella Herba (BH), Akebiae Lignum (AL) and Atractylis Rhizoma (AR) are some of the diuretic agents used in Chinese medicine and folk remedy. Water or methanol extracts of them (100mg/kg) were intravenously injected to rabbits in order to re-evaluate the effects on renal function. PR water extract elicited moderate diuresis while water extracts of BH, AL and methanol extract of AR had antidiuretic effects. Influence of PR on renal hemodynamics and $Na^+-K^+$-ATPase activity in rabbit kidney were observed in vivo and in vitro. The results were as follows: 1) Clearances of inulin and p-aminohippuric acid increased significantly after 15 minutes following the administration of PR water extract, but Na+ reabsorption rate was not changed. 2) The increase of $Na^+-K^+$-ATPase activity in renal cortex, outer and inner medulla was observed at 15 minutes after PR water fraction was given intravenously, and the change was most prominent in cortical area. 3) More than 50% of decrease in $Na^+-K^+$-ATPase activity in renal tissues was observed with PR water fraction $(10^{-2}g/ml)$ in vitro experiments. However, the inhibition of $Na^+-K^+$-ATPase activity was reversed with lower concentrations $(10^{-4}g/ml,\;10^{-6}g/ml)$ of PR water fraction in outer and inner medullary zone. These results suggest the diuretic effect of PR is due to improved renal hemodynamics, and contradictory reults concerning $Na^+-K^+$-ATPase activity require further investigation.