Fig. 1
Proposed cardioprotective signaling of OT during ischemia reperfusion (modified from reference [19]). OT acts via its G protein coupled receptors (GPCR). OT triggers the PLC-β and PI3K pathways to stimulate NO production, the regulation of ionic pumps and subsequent inhibition of the mitochondrial permeability transition pore. OT also stimulates ANP release, which in turn binds to NP receptor A to also inhibit mPTP opening. OT: oxytocin; OTR: OT receptor; PLC-β: phospholipase C type β; DAG: diacylglycerol; IP3: inositol-3-phosphate; PKC: protein kinase C; Erk1/2 : Extracellular regulated kinase 1 and 2; PI3K phosphatidylinositol-3-kinase; eNOS: endothelial nitric oxide synthase; NO: Nitric oxide; sGC: soluble guanylate cyclase; pGC: particulate guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; ROS: reactive oxygen species; mPTP: mitochondrial permeability transition pore; mitoKATP: mitochondrial ATP-dependent K+ channels; CaM: Ca2+- Calmodulin; CaMKK: CaM kinase kinase; AMPK: cAMP-activated protein kinase; NPR-A: Natriuretic peptide receptor type A. 1. NHE: exchanger Na+/H+ present on cell membrane; 2. Na+/K+ ATPase pomp; 3. Co-transporter Na+/bicarbonate; 4. NCE: exchanger Na+/Ca2+