CortisolのHenle上行脚における作用様式

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タイトル別名
  • Mode of Action of Cortisol at the Ascending Limb of the Loop of Henle
  • Cortisol ノ Henle ジョウコウキャク ニ オケル サヨウ ヨウシキ

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It is generally accepted that cortisol enhances sodium transport at the ascending limb. However, mechanism of the action has not been clearly defined. There are two possible explanations for the mode of action at the site. Cortisol may stimulate directly a pumping out sodium from the cell at the ascending limb into the peritubular fluid. The second possibility is an enhancement of sodium supply from the more proximal sites to the ascending limb, resulting in an increase of inward diffusion of sodium across the luminal membrane of the cell. Therefore, the study was undertaken on purpose to define which is the case. Two experiments were performed on 7 healthy students (age 19-21). In one experiment the subjects were fed normal sodium diets and in the other were fed low sodium diets (salt 3-4 g/day). Both diets contained 80 g of protein and were otherwise normal in composition, which were given for 2 days before experiments. 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. At 8: 30 a. m. on the day of the experiment 100 mg of cortisol was injected. Placebo experiments were performed after or before an interval of a week. Urine was collected at 60-minute intervals. All urine specimens were analyzed for sodium, potassium, chloride, urea and osmolality. Urine nonurea-solute (NUS) concentration was calculated as an index of medullary one. Cortisol injection decreased sodium excretion and the decrement was almost the same in the normal diet experiments as in the salt-depleted one. This was not attributed to an enhanced reabsorption of sodium at the distal nephrone, the mechanism of which is sodium/potassium exchange, because there was no change in potassium excretion in the experiments. It is reported that sodium transport at the ascending limb is indicated by an alteration in urine NUS concentrations, because NUS concentration in the medulla and collecting duct fluid have been shown to be the same in any plane cut perpendicular to the axis of the medulla under hydropenic conditions. Cortisol injection increased urine NUS concentrations. An increment in the salt-depleted subjects, however, was significantly less than noted in the subjects on nermal diets. This indicates that an increase in sodium transport at the ascending limb in the salt-depleted subjects is much smaller than that noted in the normal diet group. Therefore, the decrement in sodium excretion due to cortisol in salt-depleted subjects could not be explained by an increase of sodium reabsorption at the ascending limb. In addition, cortisol injection produced no significant alteration in creatinine clearance. This suggests that there was no decrement in the filtered sodium. It is apparent, therefore, that in the salt-depleted subjects cortisol injection resulted in an enhancement of sodium rebsorption at the proximal tubule, which caused sodium excretion to decrease. As above mentioned, if the mode of action of cortisol at the ascending limb is indirect one, sodium supply to the site should increase. On the contrary, it has decreased becouse of accelerated reabsorption at the proximal. tubule. It is concluded that cortisol stimulates directly an active transport of sodium at the ascending limb.

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