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Cyclic AMP antagonizes mitogen‐induced accumulation of inositol phosphates in human peripheral mononuclear leucocytes in vitro.
Author(s) -
Tits LJ,
Daul A.,
GrosseWilde H.,
Brodde OE
Publication year - 1990
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1990.tb05489.x
Subject(s) - ibmx , isoprenaline , endocrinology , medicine , peripheral blood mononuclear cell , inositol phosphate , phosphodiesterase inhibitor , biology , phosphodiesterase , in vitro , protein kinase a , potency , cyclic adenosine monophosphate , adenosine , chemistry , inositol , pharmacology , receptor , kinase , biochemistry , forskolin , enzyme , stimulation
The effect of intracellular increases of cyclic adenosine monophosphate (cAMP) on the accumulation of inositol phosphates (IPs) in response to various mitogens in vitro in human peripheral mononuclear leucocytes (MNL) was investigated. The beta‐adrenoceptor agonists inhibited mitogen‐induced IPs‐accumulation by about 30‐50% with a rank order of potency isoprenaline greater than adrenaline much greater than noradrenaline. This rank order corresponded with the order of potency of the beta‐adrenoceptor agonists to generate cAMP. The beta‐ adrenoceptor agonist‐induced inhibition of IPs‐accumulation in response to mitogen could be completely prevented by the beta 2‐adrenoceptor selective antagonist ICI 118,551, but not by the beta 1‐adrenoceptor selective antagonist CGP 20712A. Furthermore, the isoprenaline‐induced inhibition of IPs‐accumulation in response to mitogen could be enhanced by the phosphodiesterase inhibitor IBMX. We conclude that cAMP antagonizes mitogen‐induced IPs‐accumulation in human peripheral MNL in vitro.