Abstract
Inflammation plays an important role in the pathogenesis of hypertension. Innate and adaptive immune response may contribute to this process. The mechanisms implicating immune response in hypertension are still elusive. To date, the evidence originates in three major areas of data: cytokine production, central nervous system (CNS) stimulation, and kidney damage. The cytokine microenvironment can become proinflammatory and propagate low-grade inflammation, which may contribute to vascular injury and end-organ damage in hypertension. In addition, stimulation of the CNS by some stimuli (e.g., angiotensin II) causes mild hypertension that may modulate peripheral immune responses leading to aggravation of blood pressure elevation. The immune response can induce kidney injury and also interfere with sodium excretion, further contributing to elevation of blood pressure. The purpose of this review is to discuss recent data regarding the contribution of the different immune cell subsets and their response and mechanism of action in promoting hypertension and target-organ damage.
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Acknowledgments
Work from the authors’ laboratory was financed by the Canadian Institutes of Health Research (CIHR) grants 37917, 82790, and 102606, a Canada Research Chair on Hypertension and Vascular Research from CIHR/Government of Canada, and the Canada Fund for Innovation (all to ELS).
Disclosure
Conflicts of Interest: A. Leibowitz: none; E.L. Schiffrin: Advisory Board membership and honoraria from Bristol-Myers Squibb, Daiichi-Sankyo, Novartis, Takeda; research grant from Novartis; fees for educational presentations or service on speakers’ bureau from Abbott, Bristol-Myers Squibb, Daiichi-Sankyo, Novartis, and Takeda (none related to the present manuscript).
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Leibowitz, A., Schiffrin, E.L. Immune Mechanisms in Hypertension. Curr Hypertens Rep 13, 465–472 (2011). https://doi.org/10.1007/s11906-011-0224-9
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DOI: https://doi.org/10.1007/s11906-011-0224-9