Because of the possibility that proximal tubular rejection of sodium in response to extracellular fluid (ECF) expansion may be mediated by a factor activating renal cortical adenylate cyclase, we studied the response of urinary cyclic AMP to acute ECF expansion by administering 2000 ml of 0.9% NaCl over a 2-hr period. In 4 normal subjects there was a significant increase (p < 0.01) in urinary cyclic AMP, but this was associated with a fall in the serum calcium probably caused by dilution plus increased urinary loss. In 4 hypoparathyroid subjects, including one with documented pseudohypoparathyroidism, there was no change in urinary cyclic AMP, despite a greater fall in the serum calcium. In 4 normal subjects studied during a calcium infusion of 100 mg/hr, there was a 40% decrease in the urinary cyclic AMP during the calcium infusion along with no significant change following the acute ECF expansion. A significant correlation (r = 0.778, p < 0.001) was noted between the serum PTH concentration and urinary cyclic AMP. The data indicate that the increase in the urinary cyclic AMP, seen in normal subjects following acute ECF expansion, is caused by a fall in the serum calcium stimulating PTH secretion and is not related to increased proximal tubular rejection of sodium.
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Shaw et al. (1974) studied this question.