Abstract
A possible role of DA as an endogenous natriuretic hormone was reviewed under three aspects: (1) its excretion in response to saline vs. albumin-induced volume expansion, (2) the origin of urinary free DA and (3) urinary free DA excretion in an unexplained salt-retaining condition, idiopathic edema. We have shown (1) that the urinary free DA excretion increase in response to saline is specifically related to salt and does not occur when the same degree of volume expansion is induced by albumin, (2) that this increase in free DA originates in the kidney and (3) that idiopathic edema patients excrete less free DA than control subjects. It is proposed that free DA originating in the kidney is a rather sal than volume-dependent endogenous natriuretic factor. Its deficiency may contribute to excessive sodium retention in idiopathic edema. However, DA is probably not the single natriuretic hormone but a part of a natriuretic system, components of which are other renal vasodilating and natriuretic substances such as prostaglandins and kallikrein-bradykinin.
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