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. Author manuscript; available in PMC: 2011 Oct 30.
Published in final edited form as: Am J Hypertens. 2011 Jun 30;24(10):1149–1155. doi: 10.1038/ajh.2011.114

Figure 2.

Figure 2

Effect of Ang II on insulin-induced MAP kinase phosphorylation. (a,d,f) VSMCs were pretreated with Ang II (100 nmol/l) for 18 h and then exposed to 10 nmol/l insulin for the indicated times. (b,c,e,g) VSMCs were pretreated with vehicle or Ang II (100 nmol/l, 18 h) and then exposed to insulin (10 nmol/l, 5 min). Western blotting was performed with anti-IRS-1, phospho-p38MAP kinase, p38MAP kinase (a,b,c), phospho-JNK, JNK (d,e), and phospho-ERK 1/2, ERK 1/2 (f,g) antibodies. Data represent mean ± s.e. (n = 5), expressed as fold change compared with unstimulated cells. *P < 0.05 vs. control. Ang II, angiotensin II; ERK, extracellular regulated kinase; IRS-1, insulin receptor substrate-1; JNK, c-Jun N-terminal kinase; MAP, mitogen-activated protein; VSMCs, vascular smooth muscle cells.