The following studies were carried out in a case of primary aldosteronism on the diet containing 10g of NaCl and 3g of K per day.
NaCl restriction for 9 days resulted in a marked decrease of K excretion. The Cl excretion also decreased in the same manner as the Na. Despite these urinary changes, the plasma K, Cl, and CO
2 levels were essentially unchanged.
On spironolactone administration, on the other hand, plasma CO
2 fell, and K and Cl were elevated significantly, while there were a decrease of K excretion and a relative gain of Cl in excess of Na. A reduction of the urine pH was not demonstrated immediately after the beginning of spironolactone administration; acidification of the urine was gradually induced as the plasma CO
2 lowered. After cessation of spironolactone, the Cl excretion became higher than the Na, accompanying further acidification of the urine.
Although the increment of the H
+ excretion in the case of ammonium chloride loading was entirely within the normal range, the Cl excretion did not increase at least during the first 2 days.
The urinary acidification at night was shown in all the presented conditions.
On the basis of these findings, it is suggested that Cl is a critical factor governing the development and correction of metabolic alkalosis in primary aldosteronism. In addition, it is reasonable to presume that the alkaline urine in primary aldosteronism is not primarily due to aldosterone and not merely to K depletion, but to a function of the extracellular alkalosis to a certain extent.
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