Calcitonin inhibition of bone cell metabolism in vivo: an experimental study in dogs.
Calcitonin (CT) has been shown to act by decreasing the output of calcium from the bone, but the precise mechanism that brings about this change is still not fully understood. The present investigation was designed to study the effect of CT on the metablic activity of bone cells, utilizing changes in oxygen consumption and carbon dioxide production as indices of tissue metabolism. Arterio-venous gradients of calcium, inorganic phosphate, hydroxyproline, oxygen, carbon dioxide and hydrogen ions were studied across the canine femur. The results showed that the hypocalcemic action of CT was accompanied by a corresponding decrease in free hydroxyproline output from the bone, demonstrating that decreased bone resorption was responsible for the fall in plasma calcium levels. Reduced oxygen consumption and decreased carbon dioxide production by the bone showed that CT acted by inhibiting the metabolic activity of bone cells in vivo. It is speculated that CT may have acted by depressing mitochondrial respiration.
D000818:Animals; D001769:Blood; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism*; D002116:Calcitonin / Q000494:pharmacology*; D002118:Calcium / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs; D006863:Hydrogen-Ion Concentration; D006909:Hydroxyproline / Q000097:blood; D008433:Mathematics; D010100:Oxygen; D010313:Partial Pressure; D010710:Phosphates / Q000097:blood; D013997:Time Factors
D010710:Phosphates; D002245:Carbon Dioxide; D002116:Calcitonin; D006909:Hydroxyproline; D010100:Oxygen; D002118:Calcium