Abstract
A correlation between sodium balance and adrenal mineralocorticoid secretion, at least in part mediated by the renin-angiotensin system, can be regarded as established 1 . Disturbances of sodium balance are usually associated with parallel alterations in extracellular fluid volume; acutely induced alterations in extracellular fluid volume are known to be followed by appropriate change in renal excretion of water and sodium 2 . It would be logical if the natriuretic component of this renal response were partly under the control of aldosterone, and indeed changes in blood volume following infusion or hemorrhage lead to reciprocal change in blood levels of aldosterone or angiotensin 3 . Although it has been repeatedly emphasized that the renal reaction to altered aldosterone level is too slow to account for the prompt natriuresis which occurs with plasma volume expansion by infusions, a reduced level could contribute to the developed response. However, many investigators have shown that the natriuretic response to plasma-expanding infusions is not prevented by simultaneous administration of mineralocorticoids 4 . Even this does not exclude a participatory role of inhibited aldosterone secretion in short-term volume adjustments, as an initial high level of a hormone does not necessarily eliminate a response to lowering of this level, as has been reported 5 for the antidiuretic effect of vasopressin. Current emphasis on renal vascular factors as mediators of volume natriuresis 6 , and the fact that this response is little altered by renal denervation 7 , could suggest that adrenal catecholamine secretion rate might also play a part in renal volume responses. Unequivocal resolution of these questions would seem to depend on studies in adrenalectomized animals. Such studies in the dog have led to the conclusion that the adrenals are not essential to natriuretic response to plasma volume expansion 8 .
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