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KMID : 0360419740100020063
Korean Journal of Pharmacology
1974 Volume.10 No. 2 p.63 ~ p.74
Effect of Hydrocortisone infused into a Renal Artery on the Diuretic Actions of Acetazolamide and Aminophylline
Lee Jong-Hwa

Lee Duck-Hee
Cho Kyu-Chul
Abstract
This study was carried out to observe the direct effect of hydrocortisone on renal function by infusing it into a renal artery. Hydrocortisone (5mg/kg) or saline (0.5 ml/kg) was infused directly into the left renal artery of the rabbit, the right kidney was left intact to serve as a control for general action of acetazolamide (10 mg/kg) or aminophylline (10 mg/kg), which was administered intravenously 30 minutes after the direct infusion of pretreated drugs (hydrocortisone or saline). The changes of urine volume, pH, urinary excretion rates of , and the clearances of inulin and PAH were measured at an interval of 10 minutes for half an hour after the direct infusion of hydrocortisone or saline, and for one hour after intravenous administration of acetazolamide or aminophylline. The results of the experiment were as follows: 1. Significant changes in urine volume and urinary electrolytes (excreted rates of ) were observed in the hydrocortisone-infused group 10 minutes after the administration of acetazolamide, compared with the saline-infused group. Especially, the effect was more potent on the infused (left) side than on the contralateral (right) side. 2. Significant changes in urine volume and urinary electrolytes were also observed in all the aminophylline-treated groups, but no remarkable difference was noticed between the hydrocortisone-infused group and the saline-infused group, nor between the left and right sides. 3. No signicant changes in the clearances of inulin and PAH were in the infused (left) side of all the experimental groups, as compared with the contralateral (right) side. From the above results, it is obvious that hydrocortisone infused into a renal artery exerts diuretic action when administered in combination with acetazolamide, and the mechanism of action rests not on its hemodynamic change for renal blood flow, but on the potentiation of carbonic anhydrase inhibiting action. However, the exact mode of action remains yet to be clarified.
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