Abstract:
:The mechanism of the hypophosphatemic effect of thyrocalcitonin (TCT) is uncertain and may involve removal of inorganic phosphate (P1) from the plasma by heretofore unidentified organs. Rats, 192 g. thyroparathyroidectomized 16-24 h earlier, received 100 MRC mU TCT or vehicle (V) SC and 100 muCi 32PO4 iv. One h later plasma and tissue samples were collected. Compared to rats which received V, TCT-treated rats had lower plasma P1 (-0.36 plus or minus 0.08 mumol/ml, P smaller than 0.001) and Ca, higher liver P1 (+0.66 plus or minus 0.19 mumol/g, P smaller than 0.01) and unchanged red blood cell and rectus abdominus P1. TCT had no significant effect on the amount of perchloric acid soluble phosphate in any of the tissues. TCT-treated rats had lower plasma 32P1 (cpm/ml) and higher liver 32P1 (cpm/g) with no significant changes in specific activity (SA). TCT caused a small decrease in muscle 32P1 SA. There were no significant changes in the 32P (cpm/g) or 32P SA of the acid soluble phosphate fraction of any of the tissues. The results suggest that a portion of the hypophosphatemic effect of TCT can be accounted for by the increased P1 level in the liver.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Meyer RA Jr,Meyer MHdoi
10.1210/endo-96-4-1048subject
Has Abstractpub_date
1975-04-01 00:00:00pages
1048-50issue
4eissn
0013-7227issn
1945-7170journal_volume
96pub_type
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