Ca transport of sarcoplasmic reticulum during experimental uremia

Heimberg, K.-W.; Matthews, Clifford; Ritz, Eberhard

doi:10.1007/bf02546428

Cited by 3 publications

(4 citation statements)

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“…Treating the animals with 1,25(OH)2D3 returned Ca uptake values to normal (10)(11)(12)(13). These observations do not necessarily imply that the metabolite acts directly on the muscle cell, since its effect may be related to variations in Ca, PO4, or parathyroid hormone (PTH) blood levels.…”

mentioning

confidence: 76%

Effects of vitamin D3 metabolites on calcium fluxes in intact chicken skeletal muscle and myoblasts culturedin vitro

Giuliani

Boland

1984

Calcif Tissue Int

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25-hydroxycholecalciferol (25OHD3) and 1,25-dihydroxycholecalciferol (1,25(OH)2D3) at physiological concentrations exerted direct effects on Ca fluxes in cultured vitamin D-deficient chick soleus muscle and myoblasts. Isotopic desaturation curves of soleus muscle prelabeled with 45Ca indicated that the action of 25OHD3 is localized in a slow-exchangeable Ca pool where it stimulates net Ca uptake. On the other hand, the predominant effects of 1,25(OH)2D3 consist in an increase of the rate constant of Ca efflux of this pool and in an increase of net Ca uptake in a fast-exchangeable pool. 24,25-dihydroxycholecalciferal proved to be inactive on both Ca uptake and efflux. In addition, 1,25(OH)2D3 significantly increased 45Ca labeling of cultured chick myoblasts. These effects were accompanied by changes in the growth and differentiation of the cultures. The results suggest a direct involvement in vivo of 25OHD3 and 1,25(OH)2D3 on muscle cellular calcium.

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mentioning

confidence: 76%

Effects of vitamin D3 metabolites on calcium fluxes in intact chicken skeletal muscle and myoblasts culturedin vitro

Giuliani

Boland

1984

Calcif Tissue Int

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“…1,25 dihydroxycholecalciferol (1,25(OH)'`D3) may be the active metabolite on SR as nephrectomy and strontium feeding decreased Ca uptake. Dosage of the animal with 1,25(OH)2D3 reversed these changes [11][12][13][14]. Pointon and Smith [10], however, have suggested a role for 25OHD3 based on their observation that treatment with diphosphonate in vivo fails to impair SR transport.…”

Section: Phospholipidsmentioning

confidence: 92%

The effect of cholecalciferolin vivo on proteins and lipids of skeletal muscle from rachitic chicks

1983

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The protein and lipid constituents of skeletal muscle subcellular fractions isolated from chicks fed a vitamin D-deficient diet for 3 weeks and chicks replated with cholecalciferol (vitamin D3) were analyzed. Administration of the sterol markedly altered the protein composition of mitochondria. The changes were localized in the inner membranes and consisted of a modification of the relative amounts of proteins of approximate mol wt of 83,000, 58,000, 42,000, and 34,000. In addition, treatment with vitamin D3 modified the distribution pattern of components of the actomyosin contractile complex. An increase in actin and troponin C was particularly noticeable. No differences between rachitic and treated animals were detected in the protein composition of sarcoplasmic reticulum membranes and postmicrosomal soluble fraction. A significant increase in the phospholipid content of sarcoplasmic reticulum (P less than 0.05), and to a lesser extent of mitochondria, was observed in repleted chicks. The relative proportions of individual phospholipids, however, were not changed. Injection of an acute dose of cholecalciferol to chicks less severely depleted in vitamin D significantly stimulated the incorporation of 32PO4 in vivo to muscle homogenates, mitochondria, and sarcoplasmic reticulum (P less than 0.05). As the increases in specific activities of sarcoplasmic inorganic P and membrane lipid P were similar whereas that of serum remained unchanged, the results are compatible with the idea that vitamin D3 stimulates phosphate fluxes across muscle membranes. The sterol produced minor modifications in the fatty acid composition of sarcoplasmic reticulum (P less than 0.05).

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“…This effect is in agreement with previous observations. Experimental uremia impairs the ability of SR to concentrate and store calcium [18]. The kidney is the site of conversion of 25OHD3 to 1,25(OH)2D3 [28].…”

Section: Discussionmentioning

confidence: 99%

“…Administration of this metabolite to vitamin D-deficient rats increased the volume of SR as shown by stereological studies [ 17]. In exPerimental uremia calcium kinetics in the membranes is altered [18]. Treatment of the animals with 1,25(OH)2D.~ improved the kinetic parameters [19].…”

mentioning

confidence: 95%

Effect of 1,25-dihydroxycholecalciferol on sarcoplasmic reticulum calcium transport in strontium-fed chicks

Boland

Ritz

et al. 1983

Calcif Tissue Int

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Feeding of chicks with strontium, an inhibitor of 1,25-dihydroxycholecalciferol synthesis in kidney, during 7 days, significantly depressed the initial rate of calcium uptake and calcium storing capacity of sarcoplasmic reticulum membranes from skeletal muscle. Oral administration of 1,25(OH)2D3 to strontium-fed animals returned calcium transport values to normal. The changes observed could not be related to differences in the relative proportions of transport ATPase and calcium binding proteins. The results are consistent with a role of 1,25(OH)2D3 in muscle function.

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Ca transport of sarcoplasmic reticulum during experimental uremia

Cited by 3 publications

References 4 publications

Effects of vitamin D3 metabolites on calcium fluxes in intact chicken skeletal muscle and myoblasts culturedin vitro

Effects of vitamin D3 metabolites on calcium fluxes in intact chicken skeletal muscle and myoblasts culturedin vitro

The effect of cholecalciferolin vivo on proteins and lipids of skeletal muscle from rachitic chicks

Effect of 1,25-dihydroxycholecalciferol on sarcoplasmic reticulum calcium transport in strontium-fed chicks

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