Abstract
The role of cyclic AMP (adenosine 3’,5’-monophosphate) in hormone action is now quite firmly established. Abundant evidence now demonstrates that after release from an endocrine gland a hormone (first messenger) is transported to its effector cell (target) where it interacts with the adenyl cyclase system to release cyclic AMP (second messenger) which acts intracellularly to carry out the work of the hormone. In 1967, Chase and Aurbach demonstrated that urinary cyclic AMP, now known to be derived from both plasma and kidney, increased when parathormone (PTH) was administered to the rat and man. These workers also demonstrated a PTH-sensitive adenyl cyclase in the proximal tubules of the rat kidney and in fetal bone.
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