Effect of colchicine and calcitonin on calcemic response to metabolic acidosis.
To examine the mechanism responsible for enhanced calcium mobilization from bone in metabolic acidosis, we evaluated the effect of colchicine and calcitonin, two blockers of cell-mediated bone resorption, on the calcemic response to acute metabolic acidosis in thyroparathyroidectomized rats. Metabolic acidosis lasting 16 hr and induced by the feeding of NH4Cl led to a significant rise in serum calcium of 1.2 to 1.9 mg/dl. The administration of colchicine or calcitonin led to a decrement in serum calcium of 1.1 +/- 0.2 (P less than 0.01) and 0.7 +/- 0.2 mg/dl (P less than 0.05), respectively. Cyclic AMP levels in calvaria from rats with metabolic acidosis and from control rats were not different. These data suggest that mobilization of calcium from bone which occurs in metabolic acidosis is due, in part, to increased bone resorption, which is mediated by a cAMP-independent mechanism.
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D001842:Bone and Bones / Q000378:metabolism; D002116:Calcitonin / Q000494:pharmacology*; D003078:Colchicine / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D006934:Hypercalcemia / Q000097:blood*; D008297:Male; D010281:Parathyroid Hormone / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D010281:Parathyroid Hormone; D002116:Calcitonin; D000242:Cyclic AMP; D003078:Colchicine