To clarify the controversial renal action of calcitonin (CT) and a possible interrelationship between CT and parathyroid hormone, eight patients with untreated surgical hypoparathyroidism were studied. Various calcitonins, i.e. extracted porcine, synthetic porcine, synthetic human, and synthetic salmon CT in doses of 150 Medical Research Council U or 1.5 mg were infused over a 3 hr period. Subsequently, six of the same subjects received 500 USP U parathyroid extract (PTE) (Eli Lilly & Co., Indianapolis, Ind.) in 3 hr and later a combination of CT and PTE. In addition, two patients were given an infusion of ammonium phosphate with the aim of producting a phosphaturia of comparable degree as seen after CT and PTE, thus differentiating hormonal from nonhormonal influences on cation excretion. A protocol of serial clearance (C) studies using the patients as their own controls was followed. Serum and urinary inorganic phosphate (P), calcium (Ca), magnesium (Mg), sodium (Na), potassium (K), and creatinine (Cr) were determined and the clearance values calculated.

All CT peptides caused a uniform, immediate and significant increase of C_P, C_Na, C_K, C_Ca, and C_Mg, PTE evoked a rise of C_P, C_Na, and C_K, but C_Ca and C_Mg were reduced, the Ca and Na figures being not statistically significant. The administration of both CT and PTE resulted in a summation of individual hormone effects on Ca and Mg excretion. Phosphate infusion on the other hand induced an isolated phosphaturia but no concomitant changes of the urinary cations.

The hypoparathyroid data demonstrate that calcitonin enhances urinary elimination of P, Na, K, Ca, and Mg independently of parathyroid action, CT and PTE act qualitatively similarly on P, Na, and K excretion, while an antagonism seems to exist for the renal handling of Ca and Mg.