Why the study?
Emerging evidence highlights the role of immune activation in hypertension, necessitating a reconsideration of pathophysiological mechanisms to account for interactions between classical determinants and the immune system.
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Design
Review
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This review highlights the emerging understanding of neuroimmune interactions in hypertension, specifically how central nervous system areas modulate immune responses and autonomic function to regulate blood pressure.
Significance: Hypertension is a multifactorial disease ensuing from the continuous challenge imposed by several risk factors on the cardiovascular system. Classically known pathophysiological alterations associated with hypertension comprise neurogenic mechanisms dysregulating the autonomic nervous system (ANS), vascular dysfunction, and excessive activation of the renin angiotensin system. During the past few years, a considerable number of studies indicated that immune activation and inflammation also have an important role in the onset and maintenance of hypertension. Critical Issues: On these premises, it has been necessary to reconsider the pathophysiological mechanisms underlying hypertension development, taking into account the potential interactions established between classically known determinants of high blood pressure and the immune system. Recent Advances: Interestingly, central nervous system areas controlling cardiovascular functions are enriched with Angiotensin II receptors. Observations showing that these brain areas are crucial for mediating peripheral ANS and immune responses were suggestive of a critical role of neuroimmune interactions in hypertension. In fact, the ANS, characterized by an intricate network of afferent and efferent fibers, represents an intermediate between the brain and peripheral responses that are essential for blood pressure regulation. Future Directions: In this review, we will summarize studies showing how specific brain areas can modulate immune responses that are involved in hypertension. Antioxid. Redox Signal. 35, 1515–1530.
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Perrotta et al. (2021) studied this question.
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