**1. Introduction**

Despite the common acceptance that psychological stress causes disease, the biomedical populace remains skeptical of this outcome. Stress contributes to many disease processes. Exposures to chronic stress are considered the most deleterious as it leads to everlasting distortion in the emotional, physiological, and behavioral reverberation that accelerates susceptibility to and course of disease like essential hypertension. It is now well established that the total variability in the aetiology of HTN cannot be solely explained by physiological, genetic, and lifestyle factors. Several physiological and behavioural mechanisms are suggested to explain the link between

psychological stress, hypertension, and cardiovascular diseases (CVD). The hypothalamus–pituitary–adrenal axis and the sympathetic nervous system are activated by psychological stress, due to which hemodynamic and hormonal responses are generated [1]. Mimicking chronic stress by experimentally elevating glucocorticoids within the brain produces enhanced adrenocorticotropic hormone (ACTH) responses [2]. It increases both baseline arterial blood pressure [3] and blood pressure and heart responses to an acute novel stressor [4], as seen in many animal studies. There is a vast body of documentation to support the role of psychosocial factors as the primary risk for HTN [5–7]. As a result, national HTN guidelines recommend psychosocial intervention as a means to prevent or delay the onset of HTN [8–10].

Hypertension (HTN) is a rapidly pervasive condition observed in different parts of the world. It brings about a variety of chronic conditions in the human body [11] without apparently noticeable symptoms and hence is often called a silent killer [12]. It affects the overall body functioning and human life in various ways. Untreated patients with HTN have an average life expectancy between 50 and 60 years, compared with 71 years for the population at large.

What causes essential hypertension is still unknown. The intensity and duration of exposure to chronic stressors are presumed to be important determinants of risk. Effects of acute stressors on blood pressure (BP) have been demonstrated, but ongoing exposure to stress may be more plausibly linked to sustained BP elevations and hypertension incidence [5]. The effects of chronic stress in several domains are being investigated, including work-related stress, relationship stress, low socioeconomic status (SES). The adrenal gland is a major site that coordinates the stress response via the hypothalamic-pituitary–adrenal axis and the sympathetic-adrenal system. There is a fight or flight response to the stress stimulus. Due to which catecholamines are released from the adrenal medulla, they function in the neurohormonal regulation of blood pressure and have a well-established link to hypertension.

The psychological status of an individual greatly affects his physical condition. Hypertension is among the seven psychosomatic diseases for which mental aetiologies were proposed in the 1950s [13]. Studies conducted during the last decade have reported significant relationships between HT and psychological factors such as anger, anxiety, and depression. Usually, as individuals experience stress, they activate the sympathetic nervous system and the hypothalamic-pituitary–adrenal– cortical axis system. As a result of this activation, catecholamines (e.g., epinephrine and norepinephrine) and glucocorticoids (e.g., cortisol) are released, contributing to increases in blood pressure and heart rate [14]. Although the exact mechanism that explains the relationship between cardiovascular reactivity (CVR) and high blood pressure (and the subsequent development of coronary artery disease) is still under debate, research has focused on releasing catecholamines and glucocorticoids [15]. Early research in this field investigated trait anger and whether it was related to overall increased physiological reactivity [14]. These researchers assumed physiological reactivity was a person-based trait associated with a constellation of emotional, cognitive, and behavioural anger reactions. Anger could contribute to the elevation of BP directly through the psychophysiological activation and indirectly by facilitating the emergence of a coping style that contributes to the maintenance of elevated BP [16–18].

Also, anger and hostility are associated with adverse lifestyle behaviour, such as excess alcohol consumption and smoking, higher BMI values, and increased total energy intake [19], which are recognized as critical behavioural risk factors for HT and cardiovascular diseases.

*Stress-induced Anger and Hypertension: An Evaluation of the Effects of Homeopathic… DOI: http://dx.doi.org/10.5772/intechopen.104589*
