高血圧症患者におけるカリウム負荷時の尿中アルドステロン排泄量及び電解質代謝の変動について

抄録

Serum sodium and potassium levels, urinary sodium, potassium, and aldosterone excretions have been determined with or without additional oral load of 135 meq, per day of potassium chloride in normals and patients with essential and renal hypertension and primary aldosteronism on diet containing constant amounts of sodium and potassium. In most of the patients with primary aldosteronism and the other hypertensives, the urinary aldosterone excretion before potassium load was higher than in normals but no significant difference was found between the two groups. The subjects with relatively lower serum potassium levels tended to show higher urinary aldosterone excretions. It was inferred, therefore, that the hypokalemia occasionally accompanying hypertensive diseases is due to increased secretion of aldosterone. After the beginning of potassium loading the urinary aldosterone excretion rapidly increased in normals and patients with primary aldosteronism, but only gradually in the other severe hypertensives. This suggested that the adrenals of severe hypertensives have a relative autonomy on aldosterone secretion, and that, on the other hand, in the patients with primary aldosteronism the marked hypokalemia prevents the production of aldosterone and, therefore, urinary aldosterone is not always more copious in them than in the other hypertensives; for this reason the urinary aldosterone excretion rapidly increases after potassium loading.The elevation of serum potassium level was more remarkable and the rate of increase of urinary aldosterone excretion was lower during the potassium loading in the subjects showing marked reduction of blood pressure in consequence of the potassium chloride administration, than in those showing no reduction of blood pressure. This was explained as follows : the reduction of blood pressure due to potassium chloride administration prevents the increase of aldosterone secretion contrary to the stimulating action of potassium on aldosterone secretion, and a remarkable elevation of serum potassium level is induced. There was no correlation between the degree of increase of urinary sodium excretion due to potassium load and the degree of the reduction in blood pressure or the rate of increase of urinary aldosterone excretion. And thus, it was suggested that the reducing effect on blood pressure and the stimulating effect on aldosterone secretion of potassium load are not realized through the mediation of urinary loss of sodium, but directly by the action of potassium on them. The loss of sodium during potassium chloride administration was greater in all kinds of hypertensives described above than in normals.