Frequency and amplitude enhancement of calcium transients by cyclic AMP in hepatocytes.
Interactions between signalling pathways such as the cyclic AMP and the Ca2+/phosphatidylinositol pathway may occur and be of major relevance in the regulation of cell function. We demonstrate here that cyclic-AMP-dependent mechanisms cause a marked increase in frequency and peak free Ca2+ of alpha 1-receptor-induced Ca2+ transients in single hepatocytes and lower the threshold for alpha 1-receptor agonists. Adrenaline at low physiological concentrations generates alpha 1-receptor-induced Ca2+ transients, which requires activation of the beta 2-receptor signalling pathway. We conclude that an interaction between the alpha 1-receptor signalling pathway and cyclic-AMP-dependent mechanisms activated by beta 2-receptor occupation is crucial to elicit a complete adrenergic response to adrenaline at physiological concentrations in rat hepatocytes.
Schöfl
C
C
Department of Human Anatomy and Cell Biology, University of Liverpool, U.K.
Sanchez-Bueno
A
A
Brabant
G
G
Cobbold
P H
PH
Cuthbertson
K S
KS
D000331:Aequorin; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000502:physiology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D010656:Phenylephrine / Q000494:pharmacology*
D005576:Colforsin; D010656:Phenylephrine; D000331:Aequorin; D003994:Bucladesine; D000242:Cyclic AMP; D002118:Calcium