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Tumor promoter 12‐O‐tetradecanoylphorbol 13‐acetate inhibits mas /angiotensin receptor‐stimulated inositol phosphate production and intracellular Ca 2+ elevation in the 401L‐C3 neuronal cell line
Author(s) -
Jackson Trevor R.,
Hanley Michael R.
Publication year - 1989
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(89)81422-x
Subject(s) - angiotensin ii , protein kinase c , inositol phosphate , stimulation , intracellular , chemistry , receptor , endocrinology , renin–angiotensin system , medicine , 12 o tetradecanoylphorbol 13 acetate , inositol , inositol trisphosphate , phorbol , biochemistry , biology , signal transduction , blood pressure , phorbol ester
Stimulation of mas ‐oncogene transfected 401L‐C3 cells by angiotensins leads to the production of inositol phosphates. This response shows dose dependence, and has an apparent rank order of potency angiotensin III ⩾ angiotensin II ⪢ angiotensin I. Preincubation with 12‐O‐tetradecanoylphorbol 13‐acetate, for 5 min, significantly diminishes both inositol phosphate and intracellular [Ca 2+ ] responses to angiotensins, without affecting those stimulated by the endogenous bradykinin receptor. Incubation of 401L‐C3 cells with either phorbol ester or angiotensins leads to elevation of intracellular pH, implying that mas /angiotensin receptor stimulation itself leads to protein kinase C activation. These results suggest the operation of a negative feedback loop specific for the mas /angiotensin receptor signalling pathway, and which may be essential in defining the final biological output response to this receptor stimulation.