TY - JOUR
T1 - Immune mechanisms in hypertension
AU - Leibowitz, Avshalom
AU - Schiffrin, Ernesto L.
N1 - Funding Information:
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).
PY - 2011/12
Y1 - 2011/12
N2 - 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.
AB - 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.
KW - Adaptive and innate immune responses
KW - Cytokines
KW - Hypertension
KW - Immune response
KW - Inflammation
KW - Interferon
KW - Interleukins
KW - Macrophages
KW - Mechanisms
KW - T effector and T regulatory (Treg) lymphocytes
KW - Tumor necrosis factor
UR - http://www.scopus.com/inward/record.url?scp=81255157861&partnerID=8YFLogxK
U2 - 10.1007/s11906-011-0224-9
DO - 10.1007/s11906-011-0224-9
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 21842150
AN - SCOPUS:81255157861
SN - 1522-6417
VL - 13
SP - 465
EP - 472
JO - Current Hypertension Reports
JF - Current Hypertension Reports
IS - 6
ER -