scholarly journals Angiotensin II–Stimulated Induction of sis -Inducing Factor Is Mediated by Pertussis Toxin–Insensitive G q Proteins in Cardiac Myocytes

Hypertension ◽  
1999 ◽  
Vol 34 (4) ◽  
pp. 603-608 ◽  
Author(s):  
Rachel A. Hunt ◽  
G. Jayarama Bhat ◽  
Kenneth M. Baker
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Myocytes ◽  
Pertussis Toxin

scholarly journals Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro

Cell ◽  
1993 ◽  
Vol 75 (5) ◽  
pp. 977-984 ◽  
Author(s):  
Jun-ichi Sadoshima ◽  
Yuhui Xu ◽  
Henry S. Slayter ◽  
Seigo Izumo
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Myocytes

Angiotensin II Stimulates c-Jun NH 2 -Terminal Kinase in Cultured Cardiac Myocytes of Neonatal Rats

1997 ◽  
Vol 80 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Sumiyo Kudoh ◽  
Issei Komuro ◽  
Takehiko Mizuno ◽  
Tsutomu Yamazaki ◽  
Younzeng Zou ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Myocytes ◽  
Neonatal Rats

Angiotensin II regulates phosphorylation of translation elongation factor-2 in cardiac myocytes

2001 ◽  
Vol 281 (1) ◽  
pp. H161-H167 ◽  
Author(s):  
Allen D. Everett ◽  
Tamara D. Stoops ◽  
Angus C. Nairn ◽  
David Brautigan
Keyword(s):  
Protein Synthesis ◽  
Angiotensin Ii ◽  
Cardiac Myocytes ◽  
Elongation Factor ◽  
Protein Translation ◽  
Mitogen Activated Protein Kinase ◽  
Ang Ii ◽  
Elongation Factor 2 ◽  
Mitogen Activated Protein ◽  
20 Nm

Increased protein synthesis is the cardinal feature of cardiac hypertrophy. We have studied angiotensin II (ANG II)-dependent regulation of eukaryotic elongation factor-2 (eEF-2), an essential component of protein translation required for polypeptide elongation, in rat neonatal cardiac myocytes. eEF2 is fully active in its dephosphorylated state and is inhibited following phosphorylation by eEF2 kinase. ANG II treatment (10−10–10−7 M) for 30 min produced an AT1 receptor-specific and concentration- and time-dependent reduction in the phosphorylation of eEF-2. Protein phosphatase 2A (PP2A) inhibitors okadaic acid and fostriecin, but not the PP2B inhibitor FK506, attenuated ANG II-dependent dephosphorylation of eEF-2. ANG II activated mitogen-activated protein kinase, (MAPK) within 10 min of treatment, and blockade of MAPK activation with PD-98059 (1–20 nM) inhibited eEF-2 dephosphorylation. The effect of ANG II on eEF-2 dephosphorylation was also blocked by LY-29004 (1–20 nM), suggesting a role for phosphoinositide 3-kinase, but the mammalian target rapamycin inhibitor rapamycin (10–100 nM) had no effect. Together these results suggest that the ANG II-dependent increase in protein synthesis includes activation of eEF-2 via dephosphorylation by PP2A by a process that involves both PI3K and MAPK.

scholarly journals Angiotensin II induces Ca2+-dependent Cl- current in rabbit cardiac myocytes.

1993 ◽  
Vol 61 ◽  
pp. 101
Author(s):  
Hideyuki Morita ◽  
Junko Kimura ◽  
Masao Endoh
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Myocytes

Angiotensin II inhibits the electrogenic Na+/HCO3− cotransport of cat cardiac myocytes

2010 ◽  
Vol 49 (5) ◽  
pp. 812-818 ◽  
Author(s):  
Verónica C. De Giusti ◽  
Alejandro Orlowski ◽  
Ernesto A. Aiello
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Myocytes
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