title: Glia, sympathetic activity and cardiovascular disease.
abstract: 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.
authors.affiliation: Department of Clinical Pharmacology, University College London, London, WC1E 6JF, UK.
authors.forename: Nephtali
authors.initials: N
authors.lastname: Marina
authors.affiliation: School of Physiology and Pharmacology, Medical Sciences Building, Bristol Heart Institute, University of Bristol, Bristol, BS8 1TD, UK.
authors.forename: Anja G
authors.initials: AG
authors.lastname: Teschemacher
authors.affiliation: School of Physiology and Pharmacology, Medical Sciences Building, Bristol Heart Institute, University of Bristol, Bristol, BS8 1TD, UK.
authors.forename: Sergey
authors.initials: S
authors.lastname: Kasparov
authors.affiliation: Centre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology & Pharmacology, University College London, London, WC1E 6BT, UK.
authors.forename: Alexander V
authors.initials: AV
authors.lastname: Gourine
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008526:Medulla Oblongata / Q000502:physiology; D009457:Neuroglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*