Natriuretic hormone - a circulating inhibitor of sodium- and potassium-activated adenosine triphosphatase. Its potential role in body fluid and blood pressure regulation.

Expansion of the extracellular fluid volume (ECFV) promotes the release of a small molecular weight (less than or equal to 1,000 Daltons) humoral natriuretic factor. The resulting natriuresis is accompanied by inhibition of renal cortical tissue and red blood cell Na-K-ATPase activity. This transport inhibitor, presumably an acidic peptide derived from a larger precursor molecule, was so far recovered from the serum and urine of rat, dog, and man, and from renal cortical tissue homogenate. Using Sephadex G-25 gel chromatography the inhibitor is eluted in the post-salt fraction IV. Its natriuretic action is demonstrated by bioassay methods, it depresses sodium transport of isolated amphibian membranes and inhibits Na-K-ATPase enzyme activity in vitro. The inhibitor isolated from human urine binds to specific antibodies against digoxin. This natriuretic factor is absent in patients with arterial hypotension and in edematous patients with secondary aldosteronism. In contrast, high inhibitory activity is found in patients with primary aldosteronism, a condition which represents the most classical type of low renin volume-dependent hypertension. Since enzyme inhibition by this humoral endogenous agent probably extends to various Na-K-ATPase-dependent transport systems including vascular smooth muscle fibers, depression of their Na-K pump will raise intracellular concentrations of sodium and calcium and thereby induce vasoconstriction. It is therefore tempting to speculate that the natriuretic hormone plays an important role in the pathogenesis of volume-dependent arterial hypertension.