Involvement of the MEK-ERK pathway in autoantibody-induced constriction of isolated rat interlobar arteries. (A, B) Western blots for phosphorylated ERK1/2 from rat vascular smooth muscle cells stimulated with Control IgG or SRC IgG. Cells were pre-treated with (A) an AT₁RB (valsartan) or (B) an ET_A/BRB (bosentan). GAPDH served as a loading control. Blots of one representative experiment out of seven individual experiments are shown. Band intensities of ERK1/2 were divided by band intensities of GAPDH. Control IgG from each individual experiment was set to 1. n =7. (C) Contraction of rat renal interlobar artery rings upon exposure to Control IgG or SRC IgG ± MEKB expressed as % of the maximal contraction in response to 60 mM KCl. n =12. Mean±SEM. *P <0.05, **P <0.01, ***P <0.001. AT₁RB: angiotensin II type 1 receptor blocker; Control IgG: IgG isolated from healthy controls; ET_A/BRB: dual ET-1 type A and type B receptor blocker; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; MEKB: MEK blocker; MEK-ERK: mitogen-activated protein kinase-extracellular signal-regulated kinase; SRC IgG: IgG isolated from patients with scleroderma renal crisis