CALCITONIN SELECTIVELY STIMULATES 25-HYDROXYVITAMIN D3-1ALPHA-HYDROXYLASE IN PROXIMAL STRAIGHT TUBULE OF RAT-KIDNEY
CALCITONIN SELECTIVELY STIMULATES 25-HYDROXYVITAMIN D3-1ALPHA-HYDROXYLASE IN PROXIMAL STRAIGHT TUBULE OF RAT-KIDNEY
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DOI：
10.1038/291327a0
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发表时间：
1981-01-01
期刊：
影响因子：
64.8
通讯作者：
KUROKAWA, K
中科院分区：
文献类型：
--
作者：
KAWASHIMA, H;TORIKAI, S;KUROKAWA, K
25-羟基维生素D3（25（OH）D3）-1 α-羟化酶（1.先前报道，在成熟的维生素D缺乏大鼠中，（OH）酶）活性仅局限于近曲小管（PCT），并且在假定继发性甲状旁腺功能亢进的维生素D缺乏大鼠中，甲状旁腺切除术在很大程度上消除了酶活性。其他研究在胎兔肾脏的PCT和近端直小管（PST）中发现了酶活性。甲状旁腺激素和降钙素，当在体内给予时，可以刺激1 α-肾上腺素的产生。25（OH）2D 3，以及它们对维生素D缺乏大鼠中1 α-D3的体内作用。甲状腺甲状旁腺切除的维生素D缺乏大鼠中的（OH）酶是相加的，这一发现与这2种激素的不同作用部位一致。几种哺乳动物胎儿的血浆降钙素水平升高，而低钙血症维生素D缺乏大鼠的血浆降钙素水平可能较低。显然，降钙素可能负责刺激PST中的酶活性，而甲状旁腺激素主要激活1 α。（OH）酶在PCT中。为了测试这一点，降钙素对1.测定了维生素D缺乏大鼠肾单位特定节段的（OH）酶活性。显然，激素选择性地刺激1 α。（OH）酶活性的PST，而这种酶的活性是不可检测的控制维生素D缺乏的动物。
The 25-hydroxyvitamin D3 (25(OH)D3)-1.alpha.-hydroxylase (1.alpha.(OH)ase) activity was previously reported to be localized exclusively in the proximal convoluted tubules (PCT) in mature vitamin D-deficient rats and that the enzyme activity was largely abolished by parathyroidectomy in the vitamin D-deficient rats with presumed secondary hyperparathyroidism. Other studies found enzyme activity in both PCT and the proximal straight tubules (PST) of the fetal rabbit kidney. Parathyroid hormone and calcitonin, when given in vivo, can stimulate the production of 1.alpha.-25(OH)2D3 from 25(OH)D3 in vitamin D-deficient rats, and their in vivo effects on the 1.alpha.(OH)ase in thyroparathyroidectomized vitamin D-deficient rats are additive, a finding consistent with different sites of action of these 2 hormones. Plasma calcitonin levels are elevated in the fetus of several mammalian species, while they are likely to be low in hypocalcaemic vitamin D-deficient rats. Apparently, calcitonin could be responsible for stimulating enzyme activity in the PST while parathyroid hormone primarily activates 1.alpha.(OH)ase in the PCT. To test this, the effect of calcitonin on the 1.alpha.(OH)ase activity in defined nephron segments of vitamin D-deficient rats was tested. Evidently the hormone selectively stimulates 1.alpha.(OH)ase activity in the PST, whereas this enzyme activity is undetectable in control vitamin D-deficient animals.