Renal hemodynamics, water and electrolyte excretion in essential hypertension

Abstract

The fact that patients with essential hypertension show an altered renal excretory response to sodium chloride loading or under water and mannitol diuresis has been well established by several authors (1, 2, 4, 6, 7, 8, 11, 16, 17, 18) since the original study of Farnsworth and Barker (15, 16) was published in 1943. Hypertensive patients acutely eliminate a greater proportion of a salt and water load than do normotensive subjects. This renal abnormality appears to be due to an augmented tubular rejection of sodium, chloride, and water. It is still a matter of controversy whether this kind of excretory pattern is specific for essential hypertension. Of paramount importance is the question whether the phenomenon of exaggerated natriuresis in hypertensives reflects a disorder in water and mineral metabolism, which would be of interest with regard to the pathogenesis of essential hypertension, or whether hypernatriuresis is solely a consequence of the elevated arterial blood pressure. It is my purpose to review the data we have collected during the last few years, and to discuss the arguments in favour of our opinion that hypernatriuresis is a non-specific feature of essential hypertension and that it is due to the effect of high blood pressure on renal function found in arterial hypertension of any kind.