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Vol. 59, Issue 3, 576-585, March 2001
Instituto de Fisiología Celular, Universidad Nacional
Autónoma de México, México (A.G.-C., J.A.G.-S.); and
Endocrinology and Reproduction Research Branch, National Institute of
Child Health and Human Development, National Institutes of Health,
Bethesda, Maryland (A.O.-R., K.J.C.)
Desensitization and phosphorylation of the endogenous angiotensin
II AT1 receptor were studied in clone 9 liver cells.
Agonist activation of AT1 receptors blunted the response to
subsequent addition of angiotensin II. Partial inhibition of the
angiotensin II-induced calcium response was observed when cells were
pretreated with dibutyryl cyclic AMP, tetradecanoyl phorbol acetate
(TPA), vasopressin, or lysophosphatidic acid. All of these
desensitization processes were associated with receptor
phosphorylation. Angiotensin II-induced AT1 receptor
phosphorylation was partially blocked by the protein kinase C inhibitor
bisindolylmaleimide I and by phosphoinositide 3-kinase inhibitors
(wortmannin and LY294002); the actions of these inhibitors were not
additive. Pertussis toxin pretreatment of cells also partially
inhibited angiotensin II-induced AT1 receptor
phosphorylation. TPA-induced AT1 receptor phosphorylation was completely blocked by bisindolylmaleimide I. AT1
receptor phosphorylation was also induced by vasopressin and
lysophosphatidic acid, and these effects were partially inhibited by
bisindolylmaleimide I. Angiotensin II increased Akt/PKB (protein kinase
B) phosphorylation and protein kinase C membrane association.
The effect on Akt/PKB phosphorylation was blocked by phosphoinositide
3-kinase inhibitors. These findings indicate that clone 9 cells exhibit
both homologous and heterologous desensitization in association with
AT1 receptor phosphorylation. In these hepatic cells,
angiotensin II-induced receptor phosphorylation involves pertussis
toxin-sensitive and -insensitive G proteins, and is mediated in part
through protein kinase C and phosphoinositide 3-kinase.
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