• YAKHAK HOEJI
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• v.41 no.4
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• pp.498-511
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• 1997

The effects of UK 14,304, an ${\alpha}_2$-adrenergic agonist, on renal function were investigated in dogs. UK 14,304, when given intravenousely($15.0{\mu}g/kg,\;50{\mu}g/kg$), produced the increase of urine flow accompanied with the marked augmentation of free water clearance ($C_{H_2O}$) and reabsorption rates of sodium in renal tubules ($R_{Na}$), and the remarkable decrease of osmolar clearance ($C_{osm}$) and the amounts of sodium excreted in urine ($E_{Na}$). UK 14,304 given into a renal artery($1.5{\mu}g/kg,\;5.0{\mu}g/kg$) elicited the increase of urine flow with the augmentation of $C_{H_2O}$ in both kidney. UK 14,304, when administered into carotid artery($3.0{\mu}g/kg,\;10.0{\mu}g/kg$). exhibited the same aspect as shown in intravenous UK 14.304 at smaller dose than the intravenous dose. Diuretic action of intravenous UK 14,304 were produced together with increase of $C_{H_2O}$ in situation of water diuresis too, changes of renal function in this state were the increase of $C_{osm},\;E_{Na},\;and\;E_K$ (excreted amounts of potassium in urine), and the decrease of $R_{Na}\;and\;R_K$, these were different appearances from situation of saline diuresis. Diuretic action of intravenous UK 14,304 were blocked completely by post or pretreatment of yohim-bine, ${\alpha}_2$-adrenergic blocking agents, and inhibited by pretreatment of vasopressin, antidiuretic hormone. Above results suggest that UK 14,304 produces the diuretic action by the inhibition of vasopressin secretion and suppression of electrolytes reabsorption of electrolytes in renal tubules mediated with central ${\alpha}_2$-adrenoceptor in dog.

• Childhood Kidney Diseases
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• v.20 no.2
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• pp.88-91
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• 2016

Nephrogenic diabetes insipidus (NDI) can cause nonobstructive hydronephrosis. Congenital NDI (CNDI) is caused by a genetic mutation. This case report presents a 12-year-old girl who was incidentally diagnosed with nonobstructive hydronephrosis due to NDI caused by AQP2 gene mutation after being evaluated for microscopic hematuria found on routine health examination at school. The patient's medical and family history was unremarkable, and she complained of nocturia only at the time of the clinic visit. Bilateral hydronephrosis on abdominal ultrasonography prompted a water deprivation test, leading to diagnosis of NDI. Genetic study confirmed p.Asn (AAC)123Ser (AGC) in exon 2 of the AQP2 gene. Polyuria and hydronephrosis improved following arginine-vasopressin therapy. CNDI responsive to treatment should be considered as a possible cause of nonobstructive hydroureter.

• The Korean Journal of Physiology
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• v.5 no.2
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• pp.9-14
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• 1971

The direct effects of various agents on the phosphorylase activity of rat kidney was studied in vitro and the results were summarized as follows. 1. The kidney phosphorylase activity was markedly depressed by iodoacetic acid whereas it was increased by sodium azide. 2. DNP had no effect on the phosphorylase activity, while sodium cyanide slightly increased the activity of the enzyme. 3. Ouabain slightly depressed the phosphorylase activity whereas it was markedly depressed by oligomycin. 4. Vasopressin and histamine markedly increased the phosphorylase activity.

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2003.10a
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• pp.105-105
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• 2003

• The Korean Journal of Pharmacology
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• v.2 no.1 s.2
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• pp.13-16
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• 1966

The action of serotonin (5-Hydroxytryptamine) on the excretory function of the kidney was investigated in the dog, utilizing the clearance method and the stop-flow technique. It was shown that serotonin, $10{\mu}g/kg/min$, i. v., exerts a marked antidiuretic effects and elicits a marked hemodynamic changes in the kidney: a highly significant decrease of the glomerular filtration rate and a tendency of decrement in the renal plasma flow. Little change in the systemic blood pressure was noted, and the participation of the antidiuretic hormone in the antidiuretic action was ruled out by adding vasopressin to the infusion fluid. The stop-flow analysis showed that there is no evidence of altered activity in the tubules by serotonin. It was thus concluded that serotonin elicits anti diuresis in the dog by decreasing glomerular filtration rate, which results from the constriction of Vas afferens in the glomeruli.

• Journal of Yeungnam Medical Science
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• v.18 no.2
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• pp.297-301
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• 2001

The efficacy of injection sclerotherapy for treatment of acute esophageal variceal bleeding is well established. But several complications of endoscopic sclerotherapy have been reported. One of the complications is mesenteric venous thrombosis which develops when vasopressin is used for the sclerotherapy. We report a case of superior mesenteric venous thrombosis which developed after endoscopic sclerotherapy for control of esophageal variceal bleeding.

• Childhood Kidney Diseases
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• v.27 no.2
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• pp.76-81
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• 2023

Tolvaptan is a highly selective vasopressin receptor 2 antagonist that regulates cyclic adenosine monophosphate levels to inhibit both epithelial cell proliferation and chloride ion excretion, two mechanisms known to induce cyst expansion in autosomal dominant polycystic kidney disease (ADPKD). Tolvaptan is currently the preferred treatment of rapidly progressive disease ADPKD in adult patients; however, since cyst formation in ADPKD begins early in life, (frequently in utero), and significant disease progression with cyst expansion occurs in the first decade, tolvaptan may be advantageous as a preemptive treatment in children with ADPKD. Tolvaptan has already been used to successfully treat refractory edema or hyponatremia in children; this literature review provides insight into the biochemical basis of its action to contextualize its use in the pediatric population.

• Childhood Kidney Diseases
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• v.3 no.2
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• pp.209-216
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• 1999

Purpose : Nephrogenic diabetes insipidus (NDI) is a rare X-linked disorder associated with renal tubule resistance to arginine vasopressin (AVP). The hypothesis that the defect underlying NDI might be a dysfunctional renal AVPR2 has recently been proven by the identification of mutations in the AVPR2 gene in NDT patients. To investigate the association of mutations in th AVPR2 gene with NDI, we analyzed the AVPR2 gene located on the X chromosome. Methods : We have analyzed the AVPR2 gene in a kindred with X-linked NDI. The proband and proband's mother were analyzed by polymerase chain reaction-single strand conformational polymorphism(PCR-SSCP) and DNA sequencing of the AVPR2 gene. We also have used restriction enzyme analysis of genomic PCR product to evaluate the AVPR2 gene. Results : C to T transition at codon 202, predictive of an exchange of tryptophan 202 by cysteine(R202C) in the third extracellular domain was identified. This mutation causes a loss of Hae III site within the gene. Conclusion : We found a R202C missense mutation in the AVPR2 gene causing X-linked NDI, and now direct mutational analysis is available for carrier screening and early diagnosis.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.913-919
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• 2006

Background: Vasodilatory shock has been implicated in life-threatening complications after open heart surgery, where the systemic inflammatory reaction is attributed to the cardiopulmonary bypass(CPB). The secretion of arginine vasopressin(AVP) has been found to be defective in a variety of vasodilatory shock states and administration of AVP markedly improves vasomotor tone and blood pressure. So we reviewed our experience of AVP therapy in patients with vasodilatory shock following heart surgery using CPB. Material and Method: From January 2004 to July 2006, we reviewed the records of patients who received AVP therapy for vasodilatory shock following heart surgery using CPB. Vasodilatory shock was defined as a mean arterial pressure lower(MAP) than 70 mmHg, a cardiac index greater than 2.5 $L/min/m^2$, peripheral vascular resistance lower than 800 $dyn/s/cm^5$, and vasopressor requirements. The hemodynamic responses of patients who received AVP therapy for vasodilatory shock after cardiac surgery were analyzed retrospectively. Result: One hundred ninety nine open cardiac surgery patients were consecutively included in this study. Twenty two patients(11.1%) met criteria for vasodilatory shock. Despite the administration of high dose catecholamine vasopressor, all patients were hypotensive with a mean arterial pressure less than 70 mmHg. AVP therapy increased MAP from $53.3{\pm}7.4\;to\;82.0{\pm}12.0$ mmHg at 1 hour (p<0.001) and decreased other vasopressor requirements from $25{\pm}7\;to\;18{\pm}6$ at 1 hour(p<0.001) and individually maintained it for 12 hours. Conclusion: Our date suggest that AVP may be a safe and an effective vasopressor in patients with vasodilatory shock. In patients exhibiting vasodilatory shock after heart surgery, replacement of AVP increases blood pressure and reduces catecholamine vasopressor requirements.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.506-515
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• 2003

Background : A decreased level of serum arginine vasopressin(AVP) and an increased sensitivity to an exogenous AVP is expected in patients with septic shock who often require a high infusion rate of catecholamines. The goal of the study was to determine whether an exogenous AVP infusion to the patients with septic shock would achieve a significant decrement in infusion rate of catecholamine vasopressors while maintaining hemodynamic stability and adequate urine output. Method : Eight patients with septic shock who require a high infusion rate of norepinephrine had received a trial of 4-hour AVP infusion with simultaneous titration of norepinephrine. Hemodynamic parameters and urine output were monitored during the AVP infusion and the monitoring continued up to 4 hours after the AVP infusion had stopped. Results : Mean arterial pressure showed no significant changes during the study period(p=0.197). Norepinephrine infusion rate significantly decreased with concurrent AVP administration(p=0.001). However, beneficial effects had disappeared after the AVP infusion was stopped. In addition, hourly urine output showed no significant changes throughout the trials(p=0.093). Conclusion : Concurrent AVP infusion achieved the catecholamine vasopressor sparing effect in the septic shock patients, but there was no evidence of the improvement of renal function. Further study may be indicated to determine whether AVP infusion would provide an organ-protective effect to the septic shock patients.