Brain Angiotensin and Cardiovascular Reactivity to Negative and Positive Emotional Stress

Abstract

Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to negative emotional stress is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) has been recognized as an important regulator of cardiovascular reactivity. Apart from threatening events, exposure to appetitive stimuli is capable of inducing a distinct, sympathetically mediated rise in blood pressure in both animals and humans. Recent animal studies employing microinjection of AT 1 receptor antagonists directly into hypothalamic and brainstem nuclei indicate that locally released AngII acts to facilitate, through a superoxide-dependent mechanism, the pressor response to negative stress. Conversely, animal studies demonstrated that brain Ang II is less important in the regulation of cardiovascular arousal associated with positively motivated behavior, such as anticipation and consumption of palatable food. Thus, endogenous AngII in the brain appears to control the activation of central pathways primarily associated with the defense response, rather than nonspecifically modulating cardiovascular reactivity regardless of emotional valence (attraction or aversion) of stimuli. These findings may be of clinical importance as they suggest that targeted inhibition of Ang II -superoxide signaling in the brain may selectively reduce blood pressure reactivity to negative emotional stress, without affecting cardiovascular arousal associated with normal daily activities.

Circadian Differences in the Contribution of the Brain Renin-Angiotensin System in Genetically Hypertensive Mice

“…The central RAS is a well-recognized regulator of stress, acting within limbic, hypothalamic and medullary brain regions critical for the manifestation of the cardiovascular response to aversive stressors (Mayorov, 2007 ; Chen et al, 2009 ). In the present study we assessed the effect of acute ICV AT 1 receptor and ROS inhibition on the 5 min pressor response to restraint stress, as we have previously shown this response to be predominantly mediated by the SNS.…”