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. Author manuscript; available in PMC: 2018 Aug 4.
Published in final edited form as: Circ Res. 2017 Aug 4;121(4):451–468. doi: 10.1161/CIRCRESAHA.117.311170

Figure 2. The HPA axis, catecholamine surge and sympathetic and parasympathetic regulation mediate cardiac dysfunction after stroke.

Figure 2

Catecholamines act on β receptors, β receptors couple to the stimulatory G protein (Gs) and activate adenylyl cyclase (AC), and increase cytosolic cAMP. cAMP binds to the regulatory subunits of protein kinase A (PKA), which phosphorylates sarcolemmal L-type Ca2+ channels (LTCC) and sarcoplasmic phospholamban, which over loads mitochondria. Mitochondrial Ca2+ overload triggers oxidative stress, and the subsequent opening of their inner membrane permeability transition pore with ensuing osmotic swelling and loss of ATP synthesis, leads to myocardial cell death.