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The role of oxytocin in cardiovascular regulation Gutkowska J; Jankowski M; Antunes-Rodrigues JBraz J Med Biol Res 2014[Feb]; 47 (3): 206-14Studies of body volume expansion have indicated that lesions of the anteroventral third ventricle and median eminence block the release of atrial natriuretic peptide (ANP) into the circulation. Detailed analysis of the lesions showed that activation of oxytocin (OT)-ergic neurons is responsible for ANP release, and it has become clear that activation of neuronal circuitry elicits OT secretion into the circulation, activating atrial OT receptors and ANP release from the heart. Subsequently, we have uncovered the entire functional OT system in the rat and the human heart. An abundance of OT has been observed in the early development of the fetal heart, and the capacity of OT to generate cardiomyocytes (CMs) has been demonstrated in various types of stem cells. OT treatment of mesenchymal stem cells stimulates paracrine factors beneficial for cardioprotection. Cardiovascular actions of OT include: i) lowering blood pressure, ii) negative inotropic and chronotropic effects, iii) parasympathetic neuromodulation, iv) vasodilatation, v) anti-inflammatory activity, vi) antioxidant activity, and vii) metabolic effects. OT actions are mediated by nitric oxide and ANP. The beneficial actions of OT may include the increase in glucose uptake by CMs and stem cells, reduction in CM hypertrophy, oxidative stress, and mitochondrial protection of several cell types. In experimentally induced myocardial infarction in rats, continuous in vivo OT delivery improves cardiac healing and cardiac work, reduces inflammation, and stimulates angiogenesis. Because OT plays anti-inflammatory and cardioprotective roles and improves vascular and metabolic functions, it demonstrates potential for therapeutic use in various pathologic conditions.|Animals[MESH]|Atrial Natriuretic Factor/*blood[MESH]|Cardiotonic Agents[MESH]|Cell Differentiation[MESH]|Heart/*physiology[MESH]|Humans[MESH]|Myocytes, Cardiac/metabolism[MESH]|Nitric Oxide/metabolism[MESH]|Oxidative Stress/physiology[MESH]|Oxytocin/*physiology[MESH]|Rats[MESH]|Receptors, Oxytocin/*metabolism[MESH]|Signal Transduction/physiology[MESH] |
