Studies of marked and persistent sodium retention in previously fasted and sodium-deprived obese subjects.

To further delineate the effects of fasting and sodium deprivation on the handling of sodium when sodium intake is resumed, balance studies were performed on seven obese female subjects. All subjects underwent a period of total fasting, which continued for 27 to 29 days prior to resumption of sodium intake. Natriuresis in the first week of fasting and continued sodium chloride deprivation resulted in cumulative deficits of 383 +/- 47 mEq (SEM) and 371 +/- 41 mEq of sodium and chloride, respectively. Chloride space decreased from 21.2 +/- 2.7 L to 18.7 +/- 2.5 L, and aldosterone secretory rates (ASR) increased from 43 +/- 13 micrograms/24 h to 597 +/- 138 micrograms/24 h. Following resumption of sodium intake and simultaneous refeeding on low calorie diets in studies on four subjects (group I), cumulative sodium balances during the first seven days ranged from +586 mEq to +1,109 mEq; sodium retained/previously existing sodium deficit = 2.4, 3.2, 2.0, and 1.6 in the four subjects, respectively. Continued sodium retention resulted in cumulative sodium balances ranging from +670 mEq to +1,249 mEq at the end of 19 to 22 days in studies on three subjects whose cumulative sodium balance was +1,249 mEq, sodium retained/sodium deficit = 3.6. During the first five days of sodium intake and refeeding ASR decreased to 74 +/- 26 micrograms/24 h. Sodium chloride administration without refeeding in studies on three subjects (group II) also resulted in retention of more than enough sodium to replenish previously existing sodium deficits.(ABSTRACT TRUNCATED AT 250 WORDS)

The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation.

1. Studies on eight patients were performed to clarify the mechanism(s) of altered sodium metabolism and volume regulation in SIADH. The mechanism controlling water excretion was also studied to determine whether there is evidence that altered osmoregulation may be the basis for inappropriate ADH secretion in some patients. 2. These studies show that cumulative sodium balance and aldosterone secretion rates in patients with SIADH are negatively correlated with water intake. There is also a negative correlation between aldosterone secretion and urinary sodium excretion. In the absence of normal urine diluting ability, this increased excretion of sodium becomes a mechanism that allows an increased quantity of water to be excreted despite the persistence of an ADH effect on the renal tubules. 3. Within the range of hyponatremia observed in our studies, changes in serum sodium concentration were accounted for by changes in solute and water balance. One patient, who was potassium deficient during the studies, retained large quantities of sodium and potassium that could not be accounted for by an increase in either serum osmolality or body weight. These observations suggest that intracellular osmotically active solute is either lost or "inactivated" in some manner as intracellular potassium is replenished. 4. Marked impairment of urine diluting ability was demonstrated in all patients. However, two patients with SIADH associated with pulmonary tuberculosis exhibited graded responses to water loading, which suggests that ADH secretion may have been suppressed as serum osmolality was progressively reduced. Whether this can be attributed to a basic alteration or "re-setting" or osmoreceptor function, or is merely an indication that greater than normal reductions of serum osmolality are required to inhibit potent nonosmotic stimuli, remains to be determined.