Cardiovascular Action of Oxytocin

Abstract

EditorialOxytocin, a neuropeptide that participates in mammalian birth and lactation, is produced primarily in the hypothalamus. Oxytocin, acting in the central nervous system, plays an important role in a variety of complex social behaviors in mammals. Recent studies have suggested that oxytocin is endowed with plerotropic effects on cardiovascular system, intrinsic oxytocin system is critical for maintenance of cardiovascular homeostasis [1,2]. It has also been proposed that oxytocin may work directly on vascular cells to slow the progression of pathophysiological processes involved in cardiovascular diseases [3].Oxytocin is synthesized and released in the heart and the vasculature of rats [4,5]. The intrinsic oxytocin in the heart stimulates the local release of atrial natriuretic peptide (ANP) that slows the heart rate and decreases cardiac contractility [6]. Oxytocin action of cardiovascular system is mediated by oxytocin receptors, which are present in both the heart and large vessels [5]. Oxytocin receptors are members of a subclass of G-protein-coupled receptor and activation of the receptor transducer signaling via Gαq and Gαi subunits to activate phospholipase Cβ and mitogen-activated protein kinase，resulting in increased intracellular calcium concentration [7]. The expression of oxytocin and its receptor is eminent in postnatal cardiomyocytes, and decreases with age to low levels in adults [8]. However, oxytocin receptors develop in the endothelial cells at postnatal and achieve a plateau in adult rats, indicating a dynamic regulation of oxytocin system in the heart rather than constitutive expression [8]. Interestingly, the cardiac oxytocin expression in the fetal heart was upregulated by retinoic acid, a well-recognized major cardiomyogen. An oxytocin antagonist inhibited retinoic acid-mediated cardiomyocyte differentiation of embryonic stem cells, suggesting that cardiac oxytocin system play the role in retinoic acid-induced cardiomyogenesis [8].The homeostatic functions of the intrinsic cardiovascular oxytocin system are beginning to be understood. It has been proposed that balance between nitric oxide (NO) and oxidative stress is critical for maintenance of cardiovascular homeostasis [9]. NO is an important protective molecule in cardiovascular system. NO, an endogenous vasodilator, inhibits proliferation of vascular smooth muscle and aggregation of platelet and has anti-inflammatory and antiatherogenic effects [10]. We recently demonstrated that oxytocin dosedependently increased eNOS phosphorylation in HUVECs in vitro as well as in the aorta of rat ex vivo (ATVB). In the rat with myocardial infarct (MI) oxytocin reduced MI size and improved cardiac function and remodeling with increased eNOS expression in the scar area [11]. In the context of ischemia-reperfusion injury, pretreatment with oxytocin protected against ischemia-reperfusion-induced myocardial injury and ventricular arrhythmia, which appeared to be mediated by stimulation of NO and ANP synthesis/release, because the protective effect...