D
David A. Eisner
Researcher at University of Manchester
Publications - 267
Citations - 14383
David A. Eisner is an academic researcher from University of Manchester. The author has contributed to research in topics: Ryanodine receptor & Calcium. The author has an hindex of 69, co-authored 256 publications receiving 13473 citations. Previous affiliations of David A. Eisner include University of Oxford & Research Triangle Park.
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Journal ArticleDOI
How Structure, Ca Signals, and Cellular Communications Underlie Function in Precapillary Arterioles
TL;DR: Investigation of precapillary arterioles in ureter and vas deferens reveals the structural and signaling specializations underlying how blood flow is locally regulated, provides new insight into control of microcirculation, and provides a framework to explain its vulnerability to disease.
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The effects of hydrogen peroxide on intracellular calcium handling and contractility in the rat ventricular myocyte.
TL;DR: It is concluded that decreased SERCA activity is the major factor responsible for the changes of the systolic [Ca(2+)](i) transient amplitude and a mechanism for a reduction in [Ca (2+) spark frequency with no evidence for a Ca(2+) independent modification of ryanodine receptor open probability.
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The contribution of Na-Ca exchange to relaxation in mammalian cardiac muscle
TL;DR: Experiments are described that provide an estimate of the relative calcium pumping by the surface membrane and the SR and, in addition, show the importance of Na-Ca exchange.
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Ca2+ wave probability is determined by the balance between SERCA2-dependent Ca2+ reuptake and threshold SR Ca2+ content
Mathis K. Stokke,Mathis K. Stokke,Sarah J. Briston,Guro F. Jølle,Guro F. Jølle,Isma Manzoor,Isma Manzoor,William E. Louch,William E. Louch,Leiv Øyehaug,Leiv Øyehaug,Geir Christensen,Geir Christensen,David A. Eisner,Andrew W. Trafford,Ole M. Sejersted,Ole M. Sejersted,Ivar Sjaastad,Ivar Sjaastad +18 more
TL;DR: In ventricular cardiomyocytes with reduced SERCA2 abundance, Ca(2+) wave development following β-adrenergic stimulation is potentiated, and it is suggested that this is caused by a CaMKII-dependent shift in the balance betweenSERCA2-dependent Ca( 2+) reuptake and threshold SR Ca-2+) content.
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Heart failure and the ryanodine receptor: does Occam's razor rule?
TL;DR: The activity of SERCA is depressed by the accessory protein phospholamban and this inhibition is removed by phosphorylation, providing a mechanism whereby sympathetic stimulation can increase SR Ca2+ content and henceCa2+ release from the SR.