Figure 3.

Proposed mechanisms underlying angiotensin II (Ang II)-induced aortic contraction in normotensive or pressure-overloaded condition. In normotensive condition, Ang II induces aortic contraction via epidermal growth factor receptor (EGFR), Src, metalloproteinase, extracellular signal-regulated kinase 1 and 2 (Erk1/2), and Rho kinase. In pressure-overloaded condition, Ang II induces aortic contraction via EGFR, Erk1/2, Rho kinase, and Janus kinase 2 (JAK2). Moreover, Ang II-induced aortic contraction is augmented in pressure-overloaded condition probably because the protein expression of JAK2 and myosin phosphatase targeting subunit 1 is increased. AT₁R, Ang II type 1 receptor.