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Nat Rev Cardiol. 2019 Mar 20. doi: 10.1038/s41569-019-0178-1. [Epub ahead of print]

Neuroimmune crosstalk in the pathophysiology of hypertension.

Author information

1
Istituto Auxologico Italiano, IRCCS, Department of Cardiovascular, Neural and Metabolic Sciences, San Luca Hospital, Milan, Italy.
2
Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
3
Department of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy.
4
Istituto Auxologico Italiano, IRCCS, Immunology Research Laboratory, Milan, Italy.
5
Istituto Auxologico Italiano, IRCCS, Department of Cardiovascular, Neural and Metabolic Sciences, San Luca Hospital, Milan, Italy. gianfranco.parati@unimib.it.
6
Department of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy. gianfranco.parati@unimib.it.

Abstract

Hypertension is an important risk factor for cardiovascular morbidity and mortality and for events such as myocardial infarction, stroke, heart failure and chronic kidney disease and is a major determinant of disability-adjusted life-years. Despite the importance of hypertension, the pathogenesis of essential hypertension, which involves the complex interaction of several mechanisms, is still poorly understood. Evidence suggests that interplay between bone marrow, microglia and immune mediators underlies the development of arterial hypertension, in particular through mechanisms involving cytokines and peptides, such as neuropeptide Y, substance P, angiotensin II and angiotensin-(1-7). Chronic psychological stress also seems to have a role in increasing the risk of hypertension, probably through the activation of neuroimmune pathways. In this Review, we summarize the available data on the possible role of neuroimmune crosstalk in the origin and maintenance of arterial hypertension and discuss the implications of this crosstalk for recovery and rehabilitation after cardiac and cerebral injuries.

PMID:
30894678
DOI:
10.1038/s41569-019-0178-1

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