Brain angiotensin AT₁ receptors as specific regulators of cardiovascular reactivity to acute psychoemotional stress

Abstract

1. Cardiovascular reactivity, an abrupt rise in blood pressure (BP) and heart rate in response to psychoemotional stress, is a risk factor for heart disease. Pharmacological and molecular genetic studies suggest that brain angiotensin (Ang) II and AT(1) receptors are required for the normal expression of sympathetic cardiovascular responses to various psychological stressors. Moreover, overactivity of the brain AngII system may contribute to enhanced cardiovascular reactivity in hypertension. 2. Conversely, brain AT(1) receptors appear to be less important for the regulation of sympathetic cardiovascular responses to a range of stressors involving an immediate physiological threat (physical stressors) in animal models. 3. Apart from threatening events, appetitive stimuli can induce a distinct, central nervous system-mediated rise in BP. However, evidence indicates that brain AT(1) receptors are not essential for the regulation of cardiovascular arousal associated with positively motivated behaviour, such as anticipation and the consumption of palatable food. The role of central AT(1) receptors in regulating cardiovascular activation elicited by other types of appetitive stimuli remains to be determined. 4. Emerging evidence also indicates that brain AT(1) receptors play a limited role in the regulation of cardiovascular responses to non-emotional natural daily activities, sleep and exercise. 5. Collectively, these findings suggest that, with respect to cardiovascular arousal, central AT(1) receptors may be involved primarily in the regulation of the defence response. Therefore, these receptors could be a potential therapeutic target for selective attenuation of BP hyperreactivity to aversive stressors, without altering physiologically important cardiovascular adjustments to normal daily activities, sleep and exercise.

Garlic Powder Effect on Plasma Renin Activity, and Cardiovascular Effects of Intravenous Angiotensin I and Angiotensin II in Normotensive and Hypertensive Male Rats

“…Alignment of these changes in response to angiotensin I and angiotensin II indicates that the process of response to angiotensin II at the receptor's level and or mediation in response at the receptor or post-receptor levels may be affected by garlic powder. Also angiotensin II in addition to vessels can change blood pressure and heartbeat by affecting the central nervous system (24,36). This part of the findings is confirmed by garlic's effects on arterial blood pressure in normotensive and hypertensive animals.…”

Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats

“…However, AT 1 receptors are localized not only in areas related to the regulation of autonomic and endocrine control, but also in many other areas of the brain responsible for emotional, sensory and motor functions. For example central Ang II through AT 1 receptors may be a specific brain modulatory factor in the control of the reaction to stress (Mayorov, 2011;Saavedra et al, 2011). Stress can affect not only the hormonal and cardiovascular system, but also the gastric mucosal integrity and can initiate gastric mucosal damage.…”

Developmental origins of cardiovascular disease: Impact of early life stress in humans and rodents

“…It has been shown that alteration in a single acute stress response event can predict future cardiovascular disease risk (Chen et al, 2007), such as stroke (Jern et al, 1989) and hypertension (Kohan and Padilla, 1994). Acute stress can trigger autonomic and neuroendocrine-mediated changes in cardiac contractility and peripheral vascular resistance (Reich et al, 1981) and involves vasoactive mediators such as plasma endothelin (ET-1) (Fujii et al, 2005; Kaehler et al, 2002), angiotensin II (Mayorov, 2011) and corticosterone (Taniyama and Griendling, 2003; Treiber et al, 2000). …”

“…In this regard, the hypothalamic- pituitary-adrenocortical (HPA) system and the sympathetic nervous system (SNS) have received special attention. In addition, it has been shown that several vasoactive peptides such as vasopressin, endothelin-1 and angiotensin II are released secondary to behavioral stimuli, exerting amplificatory effects in cardiovascular reactivity (Aguilera and Rabadan-Diehl, 2000; Loria et al, 2010b; Mangiafico et al, 2002; Mayorov, 2011; Spieker et al, 2002; Treiber et al, 2000). Cardiovascular reactivity reflects an enhanced response in blood pressure, heart rate or other hemodynamic parameters to secondary stressors (Manuck & Krantz, 1985).…”