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The importance of bone marrow and the immune system in driving increases in blood pressure and sympathetic nerve activity in hypertension
Author(s) -
Ahmari Niousha,
Hayward Linda F.,
Zubcevic Jasenka
Publication year - 2020
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep088247
Subject(s) - immune system , neuroinflammation , bone marrow , sympathetic nervous system , homeostasis , neuroscience , inflammation , chemokine , immunology , medicine , microglia , innate immune system , biology , blood pressure
New FindingsWhat is the topic of this review? This manuscript provides a review of the current understanding of the role of the sympathetic nervous system in regulation of bone marrow‐derived immune cells and the effect that the infiltrating bone marrow cells may have on perpetuation of the sympathetic over‐activation in hypertension.What advances does it highlight? We highlight the recent advances in understanding of the neuroimmune interactions both peripherally and centrally as they relate to blood pressure control.Abstract The sympathetic nervous system (SNS) plays a crucial role in maintaining physiological homeostasis, in part by regulating, integrating and orchestrating processes between many physiological systems, including the immune system. Sympathetic nerves innervate all primary and secondary immune organs, and all cells of the immune system express β‐adrenoreceptors. In turn, immune cells can produce cytokines, chemokines and neurotransmitters capable of modulating neuronal activity and, ultimately, SNS activity. Thus, the essential role of the SNS in the regulation of innate and adaptive immune functions is mediated, in part, via β‐adrenoreceptor‐induced activation of bone marrow cells by noradrenaline. Interestingly, both central and systemic inflammation are well‐established hallmarks of hypertension and its co‐morbidities, including an inflammatory process involving the transmigration and infiltration of immune cells into tissues. We propose that physiological states that prolong β‐adrenoreceptor activation in bone marrow can disrupt neuroimmune homeostasis and impair communication between the immune system and SNS, leading to immune dysregulation, which, in turn, is sustained via a central mechanism involving neuroinflammation.