Potentiation of angiotensin II‐stimulated phosphoinositide hydrolysis, calcium mobilization and contraction of renal mesangial cells upon down‐regulation of protein kinase C

Abstract
Long‐term pretreatment of rat mesangial cells with 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) down‐regulated protein kinase C activity and potentiated the angiotensin II‐induced inositol trisphosphate (InsP3) formation. This increased response to angiotensin II occurred without a significant change in the receptor number or K d value of angiotensin II binding to the cells. The biologically inactive phorbol ester 4α‐phorbol 12,13‐di‐decanoate was without effect on angiotensin II‐stimulated InsP3 generation. Long‐term pretreatment with TPA also increased the angiotensin II‐induced mobilization of Ca2+ and the subsequent contraction of mesangial cells.

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