1968 年 9 巻 1 号 p. 3-12
During mannitol diuresis urinary potassium excretion increased sharply along with sodium excretion under the influence of a large dose of aldosterone, and it remained almost unchanged after 3 days' continuous administration of spirolactone. Plots of potassium excretion rates against sodium excretion rates during ordinary mannitol diuresis without any pretreatment distributed between the 2 extremes. The potassium excretion did not vanish even with spirolactone and at low rate of sodium excretion. This implies that urinary K/Na ratio can take any value at various aldosterone levels in the body, and it offers a poor guide for aldosterone activity without referring correspondent sodium excretion rate.
Since two regression lines representing the effects of aldosterone and spirolactone can contain plots obtained from some other types of diuresis, it is inferred that they present a common mode of renal tubular activity. Sodium in the tubular fluid is suspected to enter the tubular cell and to exchange with potassium there. Aldosterone may enhance this process. This facet of aldosterone activity seems to derange bodily homeostasis for potassium.
