Mechanism of Negative Potassium Balance in the Magnesium-Deficient Rat

Abstract

Abstract

Magnesium (Mg) deprivation leads to an increased urinary potassium excretion (U_KV) and a decreased plasma potassium (P_K) concentration. To evaluate the role of aldosterone in this process, rats were placed on a low-Mg diet (0.3 mg Mg/g diet). Group I animals received the low-Mg diet supplemented with normal Mg intake (2.6 mg Mg/g diet) while Group II animals received the low-Mg diet alone. Group III animals received the low-Mg diet plus spironolactone (10 mg/kg/day, sc). After 16 days on their respective diets, P_K was higher (4.4 ± 0.1 vs 3.6 ± 0.1 mEq/liter, P < 0.001), cumulative K balance was more positive (1.63 ± 0.31 vs −0.24 ± 0.16 mEq, P < 0.001), and plasma aldosterone concentration was lower (150 ± 16 vs 241 ± 15 ng/dl, P < 0.001) in Group I animals compared to Group II animals. P_K was returned toward control (3.9 ± 0.2 mEq/liter), positive K balance was restored (1.94 ± 0.25 mEq), while plasma aldosterone concentration remained elevated (280 ± 33 ng/dl) in Group III animals treated with spironolactone. Micropuncture studies revealed a distal tubular site for K entry in Group II animals as compared to Group I animals; this was reversed in Group III animals. It is concluded that dietary Mg deprivation produces kaliuresis, a fall in P_K and a rise in plasma aldosterone concentration. The kaliuresis and negative K balance are reversed by the administration of spironolactone. Micropuncture analysis demonstrated that the kaliuresis was due to increased K entry along the distal tubule consistent with the site of action of aldosterone.