Effect of Calciotropic Hormones and Cyclic Nucleotides on Aminoaciduria and Phosphaturia

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Abstract
Summary: Parathyroid extract (PTE), dibutyrylcyclic AMP (dbcAMP), adenosine cyclic 3':5'-monophosphate (cAMP), calcitonin (CT), and calcium chloride were infused separately into anesthetized, sham-operated, or TPTX vitamin D-fed adult rats to examine the effect of these calciotropic agents on fractional excretion (FE) of α-aminoisobutyric acid (AIB), and phosphate anion (Pi). AIB is a nonmetabolizable amino acid. Inulin clearance, FEAIB, and FEPi were stable in the intact (n = 10) and TPTX rat (n = 10). TPTX decreased FEaib, and FEPi significantly (P < 0.001 for both). PTE and dbcAMP both increased FEaib in the intact rat (P < 0.001); failure to obtain this response in the TPTX animal was a key finding. PTE and dbcAMP increased FEPi (P < 0.001) in both the intact and TPTX animal. CT was the only agent (versus PTE, dbcAMP, adenosine cyclic 3‘:5’-monophosphate, and CaCl2) to increase FEAIB (P < 0.001) in the TPTX rat; furthermore, it was the only agent that did not increase FEPi in the TPTX rat although it had hypocalcemic and hypophosphatemic effects. Changes in inulin clearance or plasma concentration of AIB, following infusion of calciotropic agents, do not explain the unique responses in FEAIB in the TPTX rat. Our findings suggest that hyperaminoaciduria induced by parathyroid hormone and cyclic nucleotide in the intact animal may be mediated by CT. Hyperphosphaturia is not a necessary response to small-dose (25 milliunits/kg.hr) infusions of CT. Speculation: Intracellular calcium in renal epithelium may be the final determinant of hyperaminoaciduria in hyperparathyroidism.