Differential activation of extracellular signal-regulated protein kinase 1/2 and p38 mitogen activated-protein kinase by AT1 receptors in vascular smooth muscle cells from Wistar–Kyoto rats and spontaneously hypertensive rats

Abstract

Angiotensin II-induced activation of vascular ERK1/2 and p38MAPK is increased in SHR. These effects are mediated via AT1 receptors, which activate Src-dependent pathways. Overexpression of c-fos mRNA in SHR is due to ERK1/2-dependent, p38MAPK-independent pathways. Our results suggest that angiotensin II activates numerous MAP kinases in VSMCs and that differential activation of these kinases may be important in altered growth signaling in VSMCs from SHR.