On the Influence of Body Water Volume and Potassium Supply on the Aldosterone Excretion in Arterial Hypertension¹

Abstract

Considerable volumes of iso-osmotic glucose solution were infused intravenously into healthy volunteers and patients with arterial hypertension. The aldosterone escretion decreased during and subsequently to the infusion in the normotensives whereas it did not change in the majority of the hypertensives. In some cases the excretion even rose.

A thiazide diuretic was given to normal subjects and to hypertensive patients on an ordinary diet and on a sodium restricted diet. In the normotensives the ensuing sodium and water loss was rapidly followed by a considerable, compensatory increase of the aldosterone excretion in the urine. The hypertensive patients, when given the thiazide derivative, lost similar amounts of sodium chloride and water, but, with only three exceptions, their aldosterone excretion did not increase. When potassium chloride was given during the thiazide treatment, wither to healthy subjects or to patients with hypertensive disease, the aldosterone excretion always became considerably augmented.

It is suggested that the aldosterone production in patients with hypertensive disease the body water volume and/or to changes in the potassium supply.