It is well established that patients with essential hypertension have an exaggerated natriuretic response to the rapid intravenous administration of sodium.1-4 While the mechanisms responsible for the enhanced natriuresis of essential hypertension remain unknown, a defect in the renal tubular capacity to conserve sodium has been proposed as a possible explanation.5
Most of the available literature relating to salt conservation in patients with hypertension is concerned with the response to chronic salt restriction. The experiments of Black6 and Renwick7 seem to offer conclusive proof that the hypertensive patient conserves sodium normally under these conditions. However, these chronic experiments may not be applicable to the problem of exaggerated natriuresis, because the latter occurs only in response to an acute stimulus for sodium excretion. The enhanced natriuretic response is a transient one and is followed by a rate of sodium excretion comparable to that of the normotensive subject.