Abstract

Abstract Renal effects of salmon calcitonin (SCT) were studied in man. The excreted fractions of filtered phosphate—(UV)(P × GFR) · PO 4 —and sodium—(UV)(P × GFR) · Na—and the urinary excretions of calcium (UV Ca ) and magnesium (UV Mg ) increased sharply during the intravenous administration of SCT and in the first following hour. Then UV Ca and UV Mg fell below their control values, (UV)(P × GFR) · PO 4 remained at a high level and (UV)(P × GFR) · Na returned to its control value or just slightly higher. The initial increases were proved to be due to SCT itself and a part of the later modifications to the release of endogenous parathyroid hormone (PTH). The secondary decreases of UV Ca and UV Mg were absent in patients with hypoparathyroidism, and coupled experiments in the same normal subjects infused with calcium, with or without SCT, showed that UV Ca , UV Mg , and (UV)(P × GFR) · PO 4 were persistently higher in the test where SCT was given, when there was no hypocalcemia. Thus, the late modifications of UV Ca and UV Mg are the consequences of the release of PTH, whereas the sustained increase of (UV)(P × GFR) · PO 4 is not entirely due to PTH but also to the direct action of SCT. Distal blockade studies which enable proximal urine to be obtained in man showed that the ratio UPO4PPO4 over UinulPinul increased rapidly after the administration of SCT, from which we can conclude that SCT brings about a rapid decrease of the proximal tubular reabsorption of phosphate. Free water clearance expressed as a fraction of creatinine clearance was measured in normal subjects whose ADH secretion was inhibited and increased markedly after the administration of SCT which can be interpreted as the consequence of the decrease of the proximal reabsorption of sodium.

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