Meyer R A, Meyer M H
Endocrinology. 1975 Apr;96(4):1048-50. doi: 10.1210/endo-96-4-1048.
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.
甲状腺降钙素(TCT)产生低磷血症效应的机制尚不确定,可能涉及迄今未明确的器官从血浆中清除无机磷酸盐(P1)。16 - 24小时前接受甲状腺甲状旁腺切除术的192克大鼠,皮下注射100 MRC mU TCT或赋形剂(V),静脉注射100 μCi 32PO4。1小时后采集血浆和组织样本。与接受赋形剂的大鼠相比,接受TCT治疗的大鼠血浆P1较低(-0.36±0.08 μmol/ml,P<0.001),血浆Ca较低,肝脏P1较高(+0.66±0.19 μmol/g,P<0.01),红细胞和腹直肌P1无变化。TCT对任何组织中高氯酸可溶性磷酸盐的量均无显著影响。接受TCT治疗的大鼠血浆32P1(cpm/ml)较低,肝脏32P1(cpm/g)较高,比活度(SA)无显著变化。TCT使肌肉32P1 SA略有下降。任何组织的酸溶性磷酸盐部分的32P(cpm/g)或32P SA均无显著变化。结果表明,TCT的部分低磷血症效应可由肝脏中P1水平升高来解释。