Activation of Akt/protein kinase B after stimulation with angiotensin II in vascular smooth muscle cells

Am J Physiol. 1999 Jun;276(6):H1927-34. doi: 10.1152/ajpheart.1999.276.6.H1927.

Abstract

Involvement of Akt/Protein kinase B (PKB), a serine/threonine kinase with a pleckstrin-homology domain, in angiotensin II (ANG II)-induced signal transduction was investigated in cultured vascular smooth muscle cells (VSMC). Stimulation of the cells with ANG II led to a marked increase in the kinase activity of Akt/PKB, which coincided with Ser-473 phosphorylation. ANG II-stimulated Akt/PKB activation was rapid, concentration dependent, and inhibited by the AT1-receptor antagonist CV-11974, but not by pertussis toxin. Akt/PKB activity was stimulated by the Ca2+ ionophore ionomycin, suggesting the possible involvement of Ca2+ in ANG II-stimulated Akt/PKB activation. However, blockade of Ca2+ mobilization by BAPTA-AM only partially inhibited ANG II-stimulated Akt/PKB activation. ANG II-stimulated Akt/PKB activation was inhibited by the tyrosine kinase inhibitors genistein and herbimycin A and by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY-294002. These results indicate that ANG II stimulates Akt/PKB activity via AT1 receptors in VSMC and that the activities of tyrosine kinase and PI3K are required for this activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology*
  • Angiotensin Receptor Antagonists
  • Animals
  • Cells, Cultured
  • Chelating Agents / pharmacology
  • Dose-Response Relationship, Drug
  • Egtazic Acid / analogs & derivatives
  • Egtazic Acid / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Activation / physiology
  • Enzyme Inhibitors / pharmacology
  • Ionomycin / pharmacology
  • Ionophores / pharmacology
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / enzymology*
  • Pertussis Toxin
  • Phosphoinositide-3 Kinase Inhibitors
  • Phosphorylation / drug effects
  • Platelet-Derived Growth Factor / pharmacology
  • Protein Serine-Threonine Kinases*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-akt
  • Rats
  • Tetradecanoylphorbol Acetate / pharmacology
  • Time Factors
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Angiotensin Receptor Antagonists
  • Chelating Agents
  • Enzyme Inhibitors
  • Ionophores
  • Phosphoinositide-3 Kinase Inhibitors
  • Platelet-Derived Growth Factor
  • Proto-Oncogene Proteins
  • Virulence Factors, Bordetella
  • Angiotensin II
  • 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
  • Egtazic Acid
  • Ionomycin
  • Pertussis Toxin
  • Protein-Tyrosine Kinases
  • Akt1 protein, rat
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Tetradecanoylphorbol Acetate