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Studies on the mechanism of inhibition of hepatic cAMP accumulation by vasopressin
Author(s) -
Morgan Noel G.,
Shipp Clanton C.,
Exton John H.
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80835-7
Subject(s) - vasopressin , trifluoperazine , forskolin , adenylate kinase , endocrinology , medicine , cyclase , glucagon , chemistry , incubation , cytosol , chlorpromazine , hormone , calmodulin , calcium , biology , stimulation , biochemistry , enzyme
Vasopressin elicited a dose‐dependent inhibition of glucagon‐induced cAMP accumulation in isolated hepatocytes. This response was not diminished by incubation of cells with the calmodulin antagonists trifluoperazine or chlorpromazine and was only slightly reduced in Ca 2+ ‐depleted hepatocytes. Half‐maximal inhibition of cAMP accumulation occurred at 8 × 10 ‐11 M vasopressin, a dose which does not increase cytosolic Ca 2+ in hepatocytes. Direct activation of adenylate cyclase by forskolin was significantly inhibited by vasopressin in Ca 2+ ‐depleted cells. It is concluded that inhibition of hormone‐induced cAMP accumulation by vasopressin in liver is not dependent on cellular Ca 2+ mobilisation but may involve direct inhibition of adenylate cyclase.