Abstract
The kidney is able to adapt to a variety of chronic changes in excretory needs, for example, to high or low sodium or potassium intake [1] and to acidosis and alkalosis [2]. One of the main functions the mammalian kidney assumes is the concentration of solutes in the urine. The diversity of mammals affords examples of renal adaptation to water conservation. Comparison among animals living in fresh water, in temperate regions, or inhabiting desert areas reveals several differences in kidney morphology and function [3]. Recent experiments have shown, not only among different species but within a given species as well, remarkable functional adaptation of the kidney to chronic variations in urine concentration. Urine concentration can be altered for sustained periods of time by modifying either antidiuretic hormone (ADH) or fluid intake. The Brattleboro rat offers a unique model in which the effects of the total absence of ADH can be studied [4]. By studying homozygous Brattleboro rats with diabetes insipidus (DI) and comparing their kidney function and morphology with that of heterozygous rats of the same strain, normal Long Evans rats (the strain from which the Brattleboro are derived), and DI rats chronically receiving antidiuretic hormone, we were able to demonstrate several features of the renal adaptation to water conservation. Several of these features were also observed in normal rats in response either to an increase or to a decrease in water intake for several weeks. These changes are described in the first part of this paper. The second part will address the mechanisms by which these changes are induced, and how they improve the urine concentrating process.
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