B. Pieske
Medical University of Graz
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Publication
Featured researches published by B. Pieske.
British Journal of Pharmacology | 2012
Michael Sacherer; Simon Sedej; Paulina Wakula; Markus Wallner; Ma Vos; Jens Kockskämper; P Stiegler; Michael Sereinigg; D. von Lewinski; Gudrun Antoons; B. Pieske; Frank R. Heinzel
BACKGROUND AND PURPOSE Ca2+ leak from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyR2s) contributes to cardiomyocyte dysfunction. RyR2 Ca2+ leak has been related to RyR2 phosphorylation. In these conditions, JTV519 (K201), a 1,4‐benzothiazepine derivative and multi‐channel blocker, stabilizes RyR2s and decrease SR Ca2+ leak. We investigated whether JTV519 stabilizes RyR2s without increasing RyR2 phosphorylation in mice and in non‐failing human myocardium and explored underlying mechanisms.
Cardiovascular Research | 2003
Horacio E. Cingolani; Néstor G. Pérez; B. Pieske; Dirk von Lewinski; María C. Camilión de Hurtado
The stretch of the cardiac muscle is immediately followed by an increase in the contraction strength after which occurs a slow force increase (SFR) that takes several minutes to fully develop. The SFR was detected in a wide variety of experimental preparations including isolated myocytes, papillary muscles and/or trabeculae, left ventricle strips of failing human myocardium, in vitro isovolumic and in vivo volume-loaded hearts. It was established that the initial increase in force is due to an increase in myofilament Ca2+ responsiveness, whereas the SFR results from an increase in the Ca2+ transient. However, the mechanism(s) for this increase in the Ca2+ transient has remained undefined until the proposal of Na+/H+ exchanger (NHE) activation by stretch. Studies in multicellular cardiac muscle preparations from cat, rabbit, rat and failing human heart have shown evidence that the stretch induces a rise in intracellular Na+ ([Na+]i) through NHE activation, which subsequently leads to an increase in Ca2+ transient via reverse-mode Na+/Ca2+ (NCX) exchange. These experimental data agree with a theoretical ionic model of cardiomyocytes that predicted an increased Na+ influx and a concurrent increase in Ca2+ entry through NCX as the cause of the SFR to muscle stretch. However, there are aspects that await definitive demonstration, and perhaps subjected to species-related differences like the possibility of an autocrine/paracrine loop involving angiotensin II and endothelin as the underlying mechanism for stretch-induced NHE activation leading to the rise in [Na+]i and reverse-mode NCX.
Frontiers in bioscience (Elite edition) | 2013
Anke Kockskämper; von Lewinski D; Danan Zhu; Jens Kockskämper; Mounir Khafaga; Albrecht Schmidt; Heiner Post; B. Pieske
Cardiovascular Research | 2014
Simon Sedej; M Matovina; Albrecht Schmidt; Senka Ljubojevic; Frank R. Heinzel; Sara Negri; Carlo Napolitano; M A Vos; Silvia G. Priori; B. Pieske
Cardiovascular Research | 2014
Uwe Primessnig; A. Hoell; Paulina Wakula; B. Pieske; Frank R. Heinzel
Journal of clinical and basic cardiology | 2012
Robert Gasser; Pätzold S; Holzwart E; Klemens Ablasser; Kraigher-Krainer E; Friehs I; Lewinski D; B. Pieske; Heinrich Mächler; Trantiner-Yates A; Tscheliessnig Kh; Harald Mangge; Porta S; Gasser S
Journal of clinical and basic cardiology | 2011
Holzwart E; Gasser S; Roessl U; Buehner A; Klemens Ablasser; Friehs I; B. Pieske; Heinrich Mächler; Yates A; Tscheliessnig Kh; Harald Mangge; Porta S; Robert Gasser
Intensivmedizin Und Notfallmedizin | 2011
D. von Lewinski; B. Pieske
Intensivmedizin Und Notfallmedizin | 2011
D. von Lewinski; B. Pieske
Journal of clinical and basic cardiology | 2010
S. Gasser; U. Roessl; E. Holzwart; Klemens Ablasser; I. Friehs; D. von Lewinski; B. Pieske; Heinrich Mächler; Trantiner-Yates A; Harald Mangge; Robert Gasser