Acute acid loads have been shown to titrate extra-and intracellular buffers (1, 2). The state of titration of these buffers is reflected by the level of serum bicarbonate. With sustained acid loading, serum bicarbonate ultimately stabilizes at some reduced level despite continuing acid retention, indicating that an additional buffer system is titrated. It has been suggested that such additional quantities of buffer could arise from the slow dissolution of bone mineral during chronic metabolic acidosis (3).The present metabolic balance studies were carried out to study further the relationship between acid retention and calcium balance during chronic ammonium chloride acidosis. MethodsWe carried out five metabolic balance studies in healthy men, who were hospitalized in the

No abstract

1. Sodium, calcium and magnesium reabsorption by the renal tubules are interrelated. 2. To determine whether the tubular transport of calcium and magnesium were influenced directly by adrenocortical hormones, clearance studies were carried out in normal adults before and after the administration of either a placebo, aldosterone or cortisol. 3. During the placebo studies urinary sodium and chloride excretion increased while potassium and net acid excretion were unaltered. 4. Following aldosterone infusion, sodium and chloride excretion fell while potassium and net acid excretion rose. 5. After cortisol infusion sodium excretion also fell but was accompanied only by a rise in potassium excretion. 6. Despite the observed changes in sodium excretion, neither placebo, aldosterone nor cortisol administration had any effect on the serum ultrafiltrate concentrations, rates of glomerular filtration or urinary excretion rates of calcium or magnesium. 7. We conclude that aldosterone and cortisol have no direct effect on renal tubular reabsorption of calcium or magnesium.