Abstract
BOTH renin and oxytocin augment the renal excretion of water, sodium, and potassium in rats. When these substances are injected simultaneously, the increase of diuresis is approximately equal to the sum of the amounts excreted when they are given separately. This effect is the same, even when the dose of renin is large enough to elicit a maximum excretory response within the first 2 h (ref. 1). Besides showing that oxytocin affects the output of electrolytes by a mechanism different from renin, these experiments would appear to support the assumption that oxytocin enhances the elimination of sodium by counteracting the effect of aldosterone. It has been shown that a dose range of 2.5–5 mu of oxytocin neutralizes the sodium-retaining activity of 1 µg of aldosterone2. Moreover, recent investigations by Bartter et al.3, Mulrow and Ganong4, and Kaplan and Bartter5 have demonstrated that renin, through its ability to release angiotensin, stimulates aldosterone secretion. In view of aldosterone's sodium-retaining potency, it was expected that this hormone would counteract the effect of either renin or oxytocin on sodium excretion. But contrary to the expectation, aldosterone was shown to facilitate the action of renin in the experiments here described.
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CROXATTO, H., LABARCA, E. & COFRÉ, G. Effects of d,l-Aldosterone on Renal Excretion of Water, Sodium, and Potassium induced by Renin. Nature 199, 182–183 (1963). https://doi.org/10.1038/199182a0
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DOI: https://doi.org/10.1038/199182a0
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