Effects of vitamin D and parathyroid hormone on muscle: potential role in uremic myopathy

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Abstract
Profound asthenia is an early and almost obligatory finding in rickets and osteomalacia caused by vitamin D deficiency, as well as in primary hyperparathyroidism. The relative roles of changes of electrolyte concentrations in tissue compartments, disturbed vitamin D metabolism, and parathyroid hormone excess have not been well delineated. In patients with primary hyperparathyroidism and secondary hyperparathyroidism associated with osteomalacia, histochemistry is consistent with primary neurogenic damage. The EMG does not indicate the pathogenetic mechanism. Biochemical studies show a direct effect of vitamin D on various aspects of muscle function: actinomyosin content (and also on extramuscular actin), impaired force generation, disturbed calcium transport by sarcoplasmic reticulum, decreased mitochondrial calcium content, and possibly impaired provision of ATP by mitochondria. Both 25-hydroxyvitamin D and 1,25,-dihydroxyvitamin D seem to have actions on muscle. Knowledge of the effects of parathyroid hormone on muscle is fragmentary, but muscle appears to possess a parathyroid hormone-responsive adenylate cyclase system. Alterations of skeletal muscle function in clinical and experimental uremia are due, at least in part, to deranged vitamin D metabolism. Changes of subcellular calcium transport in uremia are reverted by 1,25-dihydroxyvitamin D. Unregulated actinomyosin ATPase may be important for the hypercatabolism of uremia.