Neurogenic Background for Emotional Stress-Associated Hypertension

Purpose of Review The response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key...

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Bibliographic Details
Published in:	Current hypertension reports Vol. 25; no. 7; pp. 107 - 116
Main Authors:	Fontes, Marco Antônio Peliky, Marins, Fernanda Ribeiro, Patel, Tapan A., de Paula, Cristiane Amorim, dos Santos Machado, Liliane Ramos, de Sousa Lima, Érick Bryan, Ventris-Godoy, Ana Caroline, Viana, Ana Clara Rocha, Linhares, Isadora Cristina Souza, Xavier, Carlos Henrique, Filosa, Jessica A., Patel, Kaushik P.
Format:	Journal Article
Language:	English
Published:	New York Springer US 01-07-2023 Springer Nature B.V
Subjects:	Animals Blood Pressure - physiology Cardiology Family Medicine General Practice Heart Humans Hypertension Hypertension - etiology Hypothalamus Internal Medicine Medicine Medicine & Public Health Metabolic Diseases Nephrology Primary Care Medicine Psychological Distress Secondary Hypertension: Nervous System Mechanisms (M Wyss Secondary Hypertension: Nervous System Mechanisms (M Wyss, Section Editor) Section Editor Stress Sympathetic Nervous System Topical Collection on Secondary Hypertension: Nervous System Mechanisms Hypertension Anxiety Emotional stress Autonomic nervous system Sympathetic
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Summary:	Purpose of Review The response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key physiological responses and cognitive strategies, against stressor challenges. This extremely well-orchestrated response that was developed over millions of years of evolution is presently being challenged, over a short period of time. In this short review, we discuss the neurogenic background for the origin of emotional stress-induced hypertension, focusing on sympathetic pathways from related findings in humans and animals. Recent Findings The urban environment offers a variety of psychological stressors. Real or anticipatory, emotional stressors may increase baseline sympathetic activity. From routine day-to-day traffic stress to job-related anxiety, chronic or abnormal increases in sympathetic activity caused by emotional stressors can lead to cardiovascular events, including cardiac arrhythmias, increases in blood pressure and even sudden death. Among the various alterations proposed, chronic stress could modify neuroglial circuits or compromise antioxidant systems that may alter the responsiveness of neurons to stressful stimuli. These phenomena lead to increases in sympathetic activity, hypertension and consequent cardiovascular diseases. Summary The link between anxiety, emotional stress, and hypertension may result from an altered neuronal firing rate in central pathways controlling sympathetic activity. The participation of neuroglial and oxidative mechanisms in altered neuronal function is primarily involved in enhanced sympathetic outflow. The significance of the insular cortex-dorsomedial hypothalamic pathway in the evolution of enhanced overall sympathetic outflow is discussed.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23
ISSN:	1522-6417 1534-3111 1534-3111
DOI:	10.1007/s11906-023-01235-7