Abstract
Today it is well established that early life stress leads to cardiovascular programming that manifests in cardiovascular disease, but the mechanisms by which this occurs, are not fully understood. This perspective review examines the relevant literature that implicates the dysregulation of the gasomediator hydrogen sulfide and the neuroendocrine oxytocin systems in heart disease and their putative mechanistic role in the early life stress developmental origins of cardiovascular disease. Furthermore, interesting hints towards the mutual interaction of the hydrogen sulfide and OT systems are identified, especially with regards to the connection between the central nervous and the cardiovascular system, which support the role of the vagus nerve as a communication link between the brain and the heart in stress-mediated cardiovascular disease.
Highlights
The evidence that early life stress (ELS) leads to cardiovascular programming that manifests in cardiovascular disease (CVD) is incontrovertible, but the mechanisms by which this occurs are not fully understood
The gasotransmitter hydrogen sulfide (H2 S) and the neuroendocrine oxytocin (OT) systems were shown to interact and play parallel roles in the heart and brain in response to trauma, and evidence was provided to support their potential role as mediators in the ELS developmental origins of CVD
Discordant findings regarding the varied effects of OT exposure in early life and the varied responses to OT administration in individuals with ELS suggest that there is a need to better understand the discrepancy between the circulating levels of OT and the OT receptor (OTR) tissue expression levels
Summary
The significant role that early life stress (ELS) (e.g., poverty, childhood maltreatment such as physical, sexual, and psychological abuse, maternal separation and/or neglect (CM), and psychological comorbidities) plays in the development of cardio-metabolic disease has recently gained prominence [1]. Recent research has established that both physical and psychological trauma share physiological correlates [12,13] These include the OT and H2 S systems which are reported to be cardio-protective and display antioxidant and anti-inflammatory properties in models of psychological and physical trauma [12,14,15,16,17]. The purpose of this perspective is to explore the role of the H2 S and OT systems in the cardiovascular system and their mediating potential in ELS. For the purposes of clarity and simplification, the term ELS will be used on to include early life adversity, CM, and childhood trauma
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