Intermittent aldosteronism in periodic paralysis; dependence of attacks on retention of sodium, and failure to induce attacks by restriction of dietary sodium.

* This study has been supported by a grant from the office of the Surgeon General, Medical Research and Development, U.S. Army. † Howard Hughs Foundation investigator. WE have reported that spontaneous attacks of periodic paralysis are preceded by large increases of urinary aldosterone and by intense retention of sodium (Conn et al. 1956). This is followed shortly by sequestration of potassium within the body, both serum and urinary potassium falling abruptly and intensely. Serum-sodium often rises to abnormally high values as serum-potassium reaches its lowest ones. As the attack subsides a great diuresis of sodium occurs together with a less intense increase of urinary potassium. Serum-sodium and serumpotassium return to normal together. By this time urinary aldosterone has returned to base-line values. We have explored further the role of retention of sodium