Journal
EXPERIMENTAL PHYSIOLOGY
Volume 101, Issue 5, Pages 565-576Publisher
WILEY
DOI: 10.1113/EP085713
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Funding
- Wellcome Trust
- British Heart Foundation
- MRC [MR/L020661/1]
- BBSRC [BB/L019396/1]
- BBSRC [BB/L019396/1] Funding Source: UKRI
- MRC [MR/L020661/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/L019396/1] Funding Source: researchfish
- British Heart Foundation [FS/13/5/29927] Funding Source: researchfish
- Medical Research Council [MR/L020661/1] Funding Source: researchfish
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Increased activity of the sympathetic nervous system is associated with the development of cardiovascular disease and may contribute to its progression. Vasomotor and cardiac sympathetic activities are generated by the neuronal circuits located in the hypothalamus and the brainstem. These neuronal networks receive multiple inputs from the periphery and other parts of the CNS and, at a local level, maybe influenced by their non-neuronal neighbours, in particular glial cells. In this review, we discuss recent experimental evidence suggesting that astrocytes and microglial cells are able to modulate the activity of sympathoexcitatory neural networks in disparate physiological and pathophysiological conditions. We focus on the chemosensory properties of astrocytes residing in the rostral ventrolateral medulla oblongata and discuss signalling mechanisms leading to glial activation during brain hypoxia and inflammation. Alterations in these mechanisms may lead to heightened activity of sympathoexcitatory CNS circuits and contribute to maladaptive and detrimental increases in sympathetic tone associated with systemic arterial hypertension and chronic heart failure.
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