Thyrocalcitonin, EGTA, and Urinary Electrolyte Excretion (original) (raw)
Research Article Free access | 10.1172/JCI105575
Department of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa.,
Department of Pediatrics, University of Missouri, School of Medicine, Columbia, Mo.
†
Address requests for reprints to Dr. Howard Rasmussen, Dept. of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa. 19104.
*
Submitted for publication April 12, 1966; accepted January 12, 1967.
Supported by grants AM-09650, AM-09494-01, and AM-01353-08 from the National Institutes of Health.
Presented in part at the Annual Meeting of the Endocrine Society, Chicago, Ill.
Find articles by Rasmussen, H. in:JCI |PubMed |Google Scholar
Department of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa.,
Department of Pediatrics, University of Missouri, School of Medicine, Columbia, Mo.
†
Address requests for reprints to Dr. Howard Rasmussen, Dept. of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa. 19104.
*
Submitted for publication April 12, 1966; accepted January 12, 1967.
Supported by grants AM-09650, AM-09494-01, and AM-01353-08 from the National Institutes of Health.
Presented in part at the Annual Meeting of the Endocrine Society, Chicago, Ill.
Find articles by Anast, C. in:JCI |PubMed |Google Scholar
Department of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa.,
Department of Pediatrics, University of Missouri, School of Medicine, Columbia, Mo.
†
Address requests for reprints to Dr. Howard Rasmussen, Dept. of Biochemistry, University of Pennsylvania, School of Medicine, Philadelphia, Pa. 19104.
*
Submitted for publication April 12, 1966; accepted January 12, 1967.
Supported by grants AM-09650, AM-09494-01, and AM-01353-08 from the National Institutes of Health.
Presented in part at the Annual Meeting of the Endocrine Society, Chicago, Ill.
Find articles by Arnaud, C. in:JCI |PubMed |Google Scholar
Published May 1, 1967 -More info
Published May 1, 1967 -Version history
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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