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Brain angiotensin-(1–7)/Mas axis: A new target to reduce the cardiovascular risk to emotional stress
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Fig. 1
Schematic diagram based on functional and anatomic studies showing central and peripheral mechanisms by which angiotensin-(1–7) could act to attenuate the effects of emotional stress. Stressful stimuli are processed via sensorial pathways and activate brain regions that subserve emotion influencing cognition, anxiety, endocrine and autonomic responses. Centrally, Ang-(1–7), formed via ACE2, could reduce anxiety acting in the amygdala and periaqueductal gray (PAG). Reduction of anxiety leads to reduction in sympathetic outflow. Direct inhibitory actions in the hypothalamus and PAG could also reduce sympathetic outflow to target organs. Facilitation of baroreflex-induced bradycardia could offer cardiovascular protection during stress responses. Peripherally, Ang-(1–7) interference with β1-adrenergic receptors could block the direct sympathetic input to the heart reducing the cardiac risk to stress such as arrhythmogenesis. Suppression of HPA axis and stress hormones could minimize the long term effects of chronic stress such as gastric ulcerations. Possibilities are given according to the review discussion (see text for details).
Fig. 2
Diagram of the RAS pathways, only the Ang receptors that are the focus of this review are illustrated. Arrow represents the direction of the reaction; squares represent the amino acids; circles represent the enzymes; blue area represents the cytoplasm. Abbreviations: Ang I, angiotensin I; Ang II, angiotensin II; Ang III, angiotensin III; Ang IV, angiotensin IV; Ang-(1–7), angiotensin (1–7); Ang A, angiotensin A; ACE, angiotensin converting enzyme; ACE2, angiotensin converting enzyme 2; AMP, aminopeptidase; DC, decarboxylase; NEP, neutral endopeptidase (neprilysin); PEP, prolylendopeptidase.
Highlights
- •Emotional stress is considered a risk factor to several diseases.
- •Neuroendocrine and autonomic mechanisms feature the response to emotional stress.
- •Activation of ACE Ang II/AT1 receptor axis enhances responses to emotional stress.
- •Activation of ACE2/Ang-(1–7)/Mas axis attenuates responses to emotional stress.
- •Ang-(1–7)/Mas axis is a promising target to reduce the risk of stress-related diseases.
Abstract
Emotional stress is now considered a risk factor for several diseases including cardiac arrhythmias and hypertension. It is well known that the activation of neuroendocrine and autonomic mechanisms features the response to emotional stress. However, its link to cardiovascular diseases and the regulatory mechanisms involved remain to be further comprehended. The renin–angiotensin system (RAS) plays an important role in homeostasis on all body systems. Specifically in the brain, the RAS regulates a number of physiological aspects. Recent data indicate that the activation of angiotensin-converting enzyme/angiotensin II/AT1 receptor axis facilitates the emotional stress responses. On the other hand, growing evidence indicates that its counterregulatory axis, the angiotensin-converting enzyme 2 (ACE2)/(Ang)iotensin-(1–7)/Mas axis, reduces anxiety and attenuates the physiological responses to emotional stress. The present review focuses on angiotensin-(1–7)/Mas axis as a promising target to attenuate the physiological response to emotional stress reducing the risk of cardiovascular diseases.
Keywords:
Angiotensin-(1–7), MAS receptors, Emotional stress, Anxiety, Cardiovascular, NeuropeptidesTo access this article, please choose from the options below
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