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. 1967 May;46(5):746–752. doi: 10.1172/JCI105575

Thyrocalcitonin, EGTA, and Urinary Electrolyte Excretion*

Howard Rasmussen 1,2,†, Constantine Anast 1,2, Claude Arnaud 1,2
PMCID: PMC297077  PMID: 6025480

Abstract

The infusion of thyrocalcitonin (TCT) into thyroparathyroidectomized rats, given either no exogenous parathyroid hormone or a constant infusion of this hormone, leads to a transient phosphaturia and a decreased excretion of urinary magnesium, calcium, and hydroxyproline without a change in glomerular filtration rate. The changes in phosphate excretion may be due to a direct effect of the hormone upon renal tubular function or they may be a consequence of the fall in plasma calcium brought about by the action of TCT upon bone. In support of this latter alternative is the fact that the infusion of sodium ethylenebis-oxyethylenenitrilotetraäcetic acid (EGTA, a specific chelator of calcium) also leads to phosphaturia presumably as a consequence of hypocalcemia. However, EGTA infusion leads to enhanced urinary hydroxyproline excretion and sustained phosphaturia. These latter observations are interpreted to mean that alterations in the local ionic environment of osteolytic cells lead to changes in their activity and constitute a local regulatory system whose activity is modulated by the hormones, thyrocalcitonin and parathyroid hormone.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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