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Effect of 1,25-dihydroxycholecalciferol on impaired calcium transport by the sarcoplasmic reticulum in experimental uremia

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Heimberg,  K.-W.
Max Planck Institute for Medical Research, Max Planck Society;

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Agostini,  Bruno
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Hasselbach,  Wilhelm
Emeritus Group Biophysics, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Matthews, C., Heimberg, K.-W., Ritz, E., Agostini, B., Fritzsche, J., & Hasselbach, W. (1977). Effect of 1,25-dihydroxycholecalciferol on impaired calcium transport by the sarcoplasmic reticulum in experimental uremia. Kidney International, 11(4), 227-235. doi:10.1038/ki.1977.35.


Cite as: https://hdl.handle.net/21.11116/0000-0002-F755-8
Abstract
Effect of 1,25-dihydroxycholecalciferol on impaired calcium transport by the sarcoplasmic reticulum in experimental uremia. In the fragmented sarcoplasmic reticulum from skeletal muscle of rabbits with experimental uremia, defective calcium ion transport is found. An impairment of all parameters is observed (initial rate of uptake, storing capacity with and without oxalate, and concentrating ability). In vivo administration of 1,25-dihydroxychole-calciferol (1,25-(OH)2-vitamin D3)(2 × 27 ng × kg of body wt-1 × day-1 and 6 × 27 ng × kg-1 × day-1, respectively) improved the kinetic parameters. The low dose improved storing capacity, and the higher dose, in addition to the storing capacity, also corrected concentrating ability and the initial rate of uptake. It is concluded that active calcium transport in the sarcoplasmic reticulum is impaired by uremia and that this defect is responsive to the administration of 1,25-(OH)2-vitamin D3.

Effet du 1,25-dihydroxycholecalciferol sur l'altération du transport du calcium par le réticulum sarcoplasmique dans l'urémie expérimentale. Un défaut du transport du calcium est observé dans le réticulum sarcoplasmique du muscle squelettique de lapins atteints d'urémie chronique expérimentale. Une altération de tous les paramètres est observée (débit initial de captation, capacité de mise en réserve avec et sans oxalate, capacité de concentration). L'administration in vivo de 1,25-(OH)2-vitamine D3 (2 × 27 ng × kg-1 × jour-1 ou 6 × 27 ng × kg-1 × jour-1) améliore les paramètres cinétiques. La dose faible améliore la capacité de mise en réserve et la dose la plus élevée corrige, outre la capacité de mise en réserve, la capacité de concentration et le débit initial de captation. La conclusion est que le transport actif de calcium dans le réticulum sarcoplasmique est altéré par l'urémie et que ce déficit est corrigé par l'administration de 1,25-(OH)2-vitamine D3.