Abstract
Pregnancy in the rat is accompanied by enhanced reabsorption of salt and water throughout most, if not all, of the gestational period. Many mechanisms have been suggested but definitive answers are still awaited. The major area of controversy centres around the detection of changes at term. There is general agreement that, at least in mid-gestation, the increase in reabsorption can be attributed to increases in the proximal tubules, the loop of Henle and collecting duct. The contribution of the proximal tubule to the increased reabsorption at term is still uncertain. Enhanced salt and water reabsorption is demonstrated in distal nephron segments irrespective of the stage of gestation. Micropuncture and microperfusion experiments have identified increased reabsorption of water, sodium and chloride in the loop of Henle, but it appears that there is net addition of glucose, urea and potassium to the tubular fluid in this segment which, at least for potassium and glucose, offsets to some extent increased reabsorption by the proximal tubule. Altered renal handling of other solutes (uric acid, calcium and magnesium) also occurs throughout pregnancy but the mechanisms responsible and nephron sites involved remain to be investigated. Attempts to attribute altered reabsorption to direct renal effects of changes in maternal hormones are inconclusive. Prolactin mimics some of the pregnancy-associated increases in reabsorption following chronic administration to male and non-pregnant female rats. These effects might be due to a direct renal action of the hormone or even to the volume expansion following its dipsogenic action.
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