Abstract
Brain renin–angiotensin system (RAS) is significantly involved in the roles of the endocrine RAS in cardiovascular regulation. Our studies indicate that the brain RAS participates in the development of cardiac hypertrophy and fibrosis through sympathetic activation. Inhibition of sympathetic hyperactivity after myocardial infarction through suppression of the brain RAS appears beneficial. Furthermore, the brain RAS modulates the cardiovascular and fluid–electrolyte homeostasis not only by interacting with the autonomic nervous system but also by modulating hypothalamic–pituitary axis and vasopressin release. The brain RAS is also involved in the modulation of circadian rhythms of arterial pressure, contributing to non-dipping hypertension. We conclude that the brain RAS in pathophysiological states interacts synergistically with the chronically overactive RAS through a positive biofeedback in order to maintain a state of alert in diseased conditions, such as cardiac hypertrophy and failure. Therefore, targeting brain RAS with drugs such as renin or angiotensin converting enzyme inhibitors or receptor blockers having increased brain penetrability could be of advantage.
Highlights
According to the WHO report Global atlas on cardiovascular disease prevention and control, cardiovascular diseases are the leading causes of death and disability in the world
Our studies indicate that the brain renin–angiotensin system (RAS) participates in the development of cardiac hypertrophy and fibrosis through sympathetic activation
Accumulating evidence indicates that angiotensins produced locally in various brain nuclei involved in homeostasis control mainly in the hypothalamus and brain stem interact with several neurotransmitter systems to regulate cardiovascular and fluid–electrolyte homeostasis, their biology and mechanisms of action representing an active area of actual research interests (Baltatu et al, 2011; Diz et al, 2011)
Summary
According to the WHO report Global atlas on cardiovascular disease prevention and control, cardiovascular diseases are the leading causes of death and disability in the world. The brain RAS is involved in the modulation of circadian rhythms of arterial pressure, contributing to non-dipping hypertension. Several lines of evidence demonstrate that chronic over activation of the brain RAS is responsible for the development and maintenance of hypertension in several animal models of disease (Baltatu et al, 2011; Diz et al, 2011).
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