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Research Article Free access | 10.1172/JCI107879
Renal Division, Department of Medicine, University of Kentucky Medical Center, Lexington, Kentucky 40506
Find articles by Luke, R. in: JCI | PubMed | Google Scholar
Published December 1, 1974 - More info
These experiments were aimed at investigating renal behavior towards chloride, as distinct from sodium, during dietary deprivation of these ions in adrenalectomized rats. Adrenalectomized and shamoperated control rats were maintained on saline for 3 wk, then chloride conservation during a very low chloride intake was assessed both with an abundant sodium intake (as buffered sodium phosphate in the drinking water) and after subsequent withdrawal of sodium. When sodium intake was high, there was no difference in chloride conservation between adrenalectomized and control animals, and sodium balance and weight were maintained similarly in both groups. At the same time, both experimental and control rats developed significant hypokalemia and elevation of the plasma bicarbonate levels as compared to other control rats ingesting a normal diet. In another group of adrenalectomized rats sodium phosphate was withdrawn, after normal chloride conservation was observed, and the low-salt diet continued. Negative sodium balance developed and was associated with a negative chloride balance, whereas sham-operated rats continued to conserve sodium and chloride. In further studies during polyuria, both adrenalectomized and control rats developed urinary chloride concentrations of less than 1 meq/liter.
Thus adrenalectomized rats can maintain chloride balance on a low chloride, high sodium intake, in contrast to their inability to conserve sodium on a low-sodium intake. It is concluded that renal tubular reabsorption of chloride in adrenalectomized rats is adequate to establish and maintain very low urinary chloride concentrations, which may imply active chloride transport in the papillary collecting duct despite the absence of adrenocortical hormone. In addition, the typical renal response to chloride deprivation, enhanced loss of potassium and accelerated reabsorption of bicarbonate, is not dependent on adrenocortical hormones.