Abstract
We have reported previously that the 25-hydroxyvitamin D3 (25(OH)D3)-1α-hydroxylase (1α(OH)ase) activity was 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 hyperparathyroidism1. However Akiba et al.2 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 1α, 25(OH)2D3 from 25(OH)D3 in vitamin D-deficient rats3–6, and, moreover, their in vivo effects on the 1α(OH)ase in thyroparathyroidectomized vitamin D-deficient rats are additive6, a finding consistent with different sites of action of these two hormones. In addition, plasma calcitonin levels are elevated in the fetus of several mammalian species7–10, while they are likely to be low in hypocalcaemic vitamin D-deficient rats. From these observations, we hypothesized that calcitonin could be responsible for stimulating enzyme activity in the PST while parathyroid hormone primarily activates 1α(OH)ase in the PCT. To test this hypothesis, we examined the effect of calcitonin on the 1α(OH)ase activity in defined nephron segments of vitamin D-deficient rats. We report here that the hormone selectively stimulates 1α(OH)ase activity in the PST, whereas this enzyme activity is undetectable in control vitamin D-deficient animals.
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Kawashima, H., Torikai, S. & Kurokawa, K. Calcitonin selectively stimulates 25-hydroxyvitamin D3-1α-hydroxylase in proximal straight tubule of rat kidney. Nature 291, 327–329 (1981). https://doi.org/10.1038/291327a0
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DOI: https://doi.org/10.1038/291327a0
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