Cortisolの近位尿細管における作用

DOI Web Site 被引用文献1件

書誌事項

タイトル別名
  • Effect of Cortisol on the Proximal Tubule
  • Cortisol ノ キン イ ニョウ サイカン ニ オケル サヨウ

この論文をさがす

抄録

It is generally accepted that cortisol enhances sodium transport at the ascending limb and augments the sodium/potassium exchange mechanism in the late distal tubule and collecting duct. However, the influence of cortisol on the sodium transport at the proximal tubule has not been thoroughly investigated. In the studies to be reported here, we have attenpted to pursuit the mode of action of cortisol at the proximal tubule with the assumptions that enhancement of sodium transport at the ascending limb due to cortisol could be suppressed by ethacrynic acid and sodium/potassium exchange mechanism at the late distal tubule by triamterene. Six healthy students (age 29-21) Were supplemented with large amount of salt (30 g/day) for 2 days in advance. All studies were performed under maximally hydropenic states after a 14-hour fast and 11 hours after the intramuscular injection of 5 U. of vasopressin tannate in oil. Two studies were performed on all subjects. In one experiment cortisol was administrered and in the other a placebo injection was given. At 8:00 a. m. on the day of the experiment 100 mg of cortisol was injected intravenously and 25 mg of ethacrynic acid and 50 mg of triamterene were given perorally 30 minutes later. Urine was collected at 60-minute intervals before and after administration of cortisol. All urine specimens were analyzed for sodium, potassium, chloride, urea and osmolality. Osmolalities were determined with a Fisk osmometer. In addition, nonurea-solute concentration was calculated as an index of medullary nonureasolute concentration. Because of administration of ethacrynic acid and triamterene, urine volume markedly increased, which, however, was not influecced by cortisol. On the contrary, the increment in sodium excretion was significantly less after cortisol than that noted in the placebo studies (p<0.02). Potassium excretion rose slightly but significantly after cortisol administration (p<0.01). Since the small increment was not enough to explain the total amount of decrease in sodium excretion, it seemed apparent that the enhancement of sodium/potassium exchange mechanism after cortisol was sufficiently inhibited, although not completely. Ethacrynic acid administration resulted in the marked decrease in non-urea solute concentration even in the cortisol studies, suggesting that active transport of sodium at the ascending limb was almost completely abolished. In addition, the mean change of glomerullar filtration rate was not statistically significant and was within the expected experimental error. Therefore, this study indicates that augmented proximal reabsorption contributes mostly to the decrement in sodium excretion after cortisol administration in the present experimental conditions.

収録刊行物

被引用文献 (1)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ