Increasing cAMP antagonizes hypertrophic response to angiotensin II without affecting Ras and MAP kinase activation in vascular smooth muscle cells.

Abstract:

:Angiotensin II (Ang II), a potent hypertrophic factor for vascular smooth muscle cells (VSMC), induces activation of the ras proto-oncogene product (Ras) and mitogen-activated protein (MAP) kinases, and tyrosine phosphorylation of a focal adhesion-associated protein, paxillin. Forskolin, a direct activator of adenylate cyclase, and dibutyryl cAMP (Bt2 cAMP), a membrane permeable cAMP analogue, potently inhibited Ang II-stimulated protein synthesis. However, they did not inhibit Ang II-induced activation of Ras and MAP kinases. Although both forskolin and Bt2 cAMP potently reduced background tyrosine phosphorylation of paxillin, they allowed Ang II to induce the same reaction. These results indicate that increasing cAMP antagonizes the hypertrophic response to Ang II without affecting Ras and MAP kinase activation in VSMC and suggest that it does not interrupt signaling from the Ang II receptor to focal adhesions.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Takahashi T,Kawahara Y,Okuda M,Yokoyama M

doi

10.1016/s0014-5793(96)01145-3

subject

Has Abstract

pub_date

1996-11-11 00:00:00

pages

89-92

issue

1

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(96)01145-3

journal_volume

397

pub_type

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