Garland, Chris - University of Oxford - Department of Pharmacology

个人简介

Professor Chris Garland joined the department in 2008. He received a BSc in Physiology & Biochemistry from the University of Southampton and then a PhD in Physiology from the University of London, after studying the influence of autonomic nerves on the sensitivity of arterial smooth muscle with WR Keatinge at the Royal London Hospital Medical School. This was followed by an NIH Postdoctoral Fellowship in Pharmacology at the University of Vermont, USA. Professor Garland returned to the UK on a Wellcome Trust Fellowship in Mental Health, and was then appointed lecturer in pharmacology at the University of Southampton, moving to Bristol in 1993, as Senior Lecturer then Reader in Pharmacology. He was then awarded a personal chair in Cardiovascular Pharmacology. He moved to the Statutory Chair of Pharmacology at the University of Bath in 2000, becoming head of pharmacology in the Department of Pharmacy & Pharmacology, moving to Oxford in 2008. Professor Garland is a Fellow of the British Pharmacological Society and was an Editor of the British Journal of Pharmacology between 1992-1996. In 2007, he was the BPS/AstraZenaca Indian visitor. He has held visiting professorships in the Department of Pharmacology at Monash University, Australia and the National Academy of Sciences, Taiwan and is currently a member of the MRC Molecular and Cellular Medicines Board. He was recently awarded the 2009 JR Vane Medal by the British Pharmacological Society, for outstanding contributions to cardiovascular pharmacology, and a Royal Society Wolfson Research Merit Award in 2010.

研究领域

Professor Garland’s research investigates the mechanisms responsible for controlling the tone of vascular smooth muscle cells. Changes in smooth muscle tone regulate the diameter of small 'resistance' arteries, and thereby control blood pressure and flow within the body. The principal focus of the vascular pharmacology group in Oxford is discovering how endothelial cells (a monolayer of cells lining all blood vessels in the body) regulate artery diameter and how this control is disrupted by disease. The group applies an integrative approach, using mainly electrophysiological and live cell imaging in pressurized small arteries and arterioles. Fundamental contributions have been made in the EDHF area. EDHF or endothelium-dependent hyperpolarizing factor describes a pathway predominant in resistance arteries and involving spread of hyperpolarization from endothelium to smooth muscle to increase artery diameter. After discovering that the hyperpolarization reflects activation KCa2.3 and KCa3.1 channels, and that these K-channels are restricted to endothelial cells, recent work has shown the channels are focused within membrane microdomains. Current research is probing the cellular signalling mechanisms responsible for differentially regulating each channel type.

近期论文

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Bagher, P and Garland, CJ (2014) Scaffolding builds to reduce blood pressure Dora, KA and Garland, CJ (2013) Linking hyperpolarization to endothelial cell calcium events in arterioles. Bagher, P, Beleznai, T, Kansui, Y, Mitchell, R, Garland, CJ, and Dora, KA (2012) Low intravascular pressure activates endothelial cell TRPV4 channels, local Ca2+ events, and IKCa channels, reducing arteriolar tone. McNeish, AJ, Jimenez-Altayo, F, Cottrell, GS, and Garland, CJ (2012) Statins and selective inhibition of rho kinase protect small conductance calcium-activated potassium channel function (k(ca)2.3) in cerebral arteries. Garland, CJ, Yarova, PL, Jimenez-Altayo, F, and Dora, KA (2011) Vascular hyperpolarization to beta-adrenoceptor agonists evokes spreading dilatation in rat isolated mesenteric arteries. Garland, CJ, Hiley, CR, and Dora, KA (2011) EDHF: spreading the influence of the endothelium. Yuill, KH, Yarova, P, Kemp-Harper, BK, Garland, CJ, and Dora, KA (2011) A novel role for HNO in local and spreading vasodilatation in rat mesenteric resistance arteries. McNeish, AJ, Altayo, FJ, and Garland, CJ (2010) Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat. Garland, CJ (2010) Compromised vascular endothelial cell SK(Ca) activity: a fundamental aspect of hypertension? Yuill, KH, McNeish, AJ, Kansui, Y, Garland, CJ, and Dora, KA (2010) Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels.