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  • Title: Effect of adrenalectomy on medullary collecting-duct function in rats before and during blood volume expansion.
    Author: Sonnenberg H.
    Journal: Pflugers Arch; 1977 Mar 11; 368(1-2):55-62. PubMed ID: 558599.
    Abstract:
    Adrenalectomized rats, kept on tap water for 3 days and infused with the glucocorticoid dexamethasone during the experiment, were compared to similarly treated sham-operated rats. Using the microcatheterization technique, reabsorption of fluid, sodium and potassium in the medullary collecting duct was studied before and after infusion of donor blood (2.3% of body weight). Before intravascular volume expansion sodium excretion in adrenalectomized rats was greater than in sham-operated ones. Extensive overlap between the two groups made this difference not statistically significant. However, the fraction of filtered sodium excreted was significantly greater after adrenalectomy, indicating the expected tubular transport defect. Fluid reabsorption from the medullary collecting-duct system was comparable in both series. Adrenalectomy did not inhibit net sodium reabsorption from the inner medullary duct, although reduction of Na transport in the outer medullary collecting system could be inferred. Renal excretion of potassium was not associated with net K secretion in the collecting duct in either group. During hypervolemia induced by intravenous infusion of donor blood, marked diuresis, natriuresis and kaliuresis were observed in all animals, associated with inhibition of net fluid and sodium reabsorption along the collecting system in both inner and outer medulla. Small, but statistically significant secretion of potassium became evident. The relatively reduced renal response in adrenalectomized animals could be attributed in part to a decreased filtered load compared to sham-operated rats. It is concluded: (1) that lack of mineralocorticoid does not prevent the normal fluid and sodium reabsorption from the lumen of the inner medullary collecting system, and (2) that the inhibition of this reabsorption consequent to hypervolemia is independent of changes in plasma aldosterone levels.
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