Glia, sympathetic activity and cardiovascular disease. Issue 5 (9th April 2016)

• Record Type: Journal Article
• Authors: Marina, Nephtali; Teschemacher, Anja G.; Kasparov, Sergey; Gourine, Alexander V.
• Is Part Of: Experimental physiology. Volume 101:Issue 5(2016:May)
• Page Start: 565
• Page End: 576
• Publication Date: 2016-04-09
• Subjects: Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/EP085713
• Languages: English
• ISSNs: 0958-0670

Abstract

Abstract : Dr Marina is a cardiovascular neuroscientist based in the University College London Centre for Cardiovascular and Metabolic Neuroscience. He obtained a medical degree and a PhD in Neuroscience from the National University of Mexico. He is currently a British Heart Foundation Intermediate Basic Science Research Fellow. His research interests lie in the role of glial cells in the control of sympathetic function and their contribution to the pathogenesis of arterial hypertension and heart failure. Abstract : New Findings: What is the topic of this review? In this review, we discuss recent findings that provide a novel insight into the mechanisms that link glial cell function with the pathogenesis of cardiovascular disease, including systemic arterial hypertension and chronic heart failure. What advances does it highlight? We discuss how glial cells may influence central presympathetic circuits, leading to maladaptive and detrimental increases in sympathetic activity and contributing to the development and progression of cardiovascular disease. 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, may be 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.