抄録
Epinephrine or carbachol, alone or together with parathyroid hormone (PTH) orcalcitonin, was added into the incubation of young rat tibia and cyclic AMP as wellas cyclic GMP in the tissue was determined. Epinephrine induced a dose related andrapid increase of cyclic AMP probably through mechanism different from that ofPTH or calcitonin. The effect of these hormones to increase cyclic AMP was additiveto the effect of maximal dose of epinephrine and, in contrary to epinephrine effect, was not influenced by propranolol. Carbachol induced a dose-related and rapidincrease of cyclic GMP in bone. The effect of carbachol was completely abolishedby adding atropine or tetracaine. A marked increase of cyclic GMP was also inducedby NaN3. There was no reciprocal relationship between the levels of cyclic AMPand cyclic GMP. The increase of cyclic GMP by carbachol was unaffected by theincrease of cyclic AMP induced by PTH, and the increase of cyclic AMP by PTHor calcitonin was the same in the presence or absence of carbachol at the dosemaximally effective to increase cyclic GMP.
The results indicate the presence in bone of adrenergic and cholinergic receptorsites, and possible regulation of bone cell activity by these nervous systems throughcyclic AMP and cyclic GMP. Though the regulation of the cyclic nucleotides contentin bone by these neurotransmitters appeared to be through mechanism independentof PTH or calcitonin action, it seems worth-while to study further how these neurotransmittersby themselves or in concert with these hormones act on the various aspects of bone cell function.
