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J Family Med Prim Care
August 2024
Department of Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, Delhi, India.
Hippokratia
January 2022
Second Department of Cardiology and Michaelidion Cardiac Center, Medical School University of Ioannina, Ioannina, Greece.
Background: Ivabradine, an agent lowering the heart rate, acting as a funny current () specific inhibitor, is responsible for the sinoatrial node's spontaneous depolarization. According to current guidelines, it is indicated in specific heart failure populations and as a second-line treatment option to improve angina in chronic coronary syndromes.
Review Of Literature: The role of ivabradine in the setting of ventricular arrhythmias has been studied in both experimental and clinical studies.
Cell Calcium
December 2019
Department of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, 3000 Arlington Ave. MS-1010, Toledo, OH 43614, USA. Electronic address:
Na/K-ATPase (the sodium pump) was discovered in the 1950s as the plasma membrane enzyme that carries out the coupled active transports of Na and K across the membranes of nearly all eukaryotic cells. It was not until the 1990s when it was shown that besides pumping ions, Na/K-ATPase is also capable of stimulus-induced interactions with neighboring proteins that lead to activations of signal transduction pathways causing cell growth. This article is an attempt to review the progress of the research on these signaling functions of sodium pump during the past 2-3 decades.
View Article and Find Full Text PDFPharmacol Res Perspect
August 2019
Department of Cancer Biology, College of Medicine and Life Sciences University of Toledo Toledo Ohio.
The sodium pump (Na/K-ATPase) is a plasma membrane enzyme that transports Na and K against their physiological gradients in most eukaryotic cells. Besides pumping ions, the enzyme may also interact with neighboring proteins to activate cell signaling pathways that regulate cell growth. Digitalis drugs, useful for the treatment of heart failure and atrial arrhythmias, inhibit the pumping function of Na/K-ATPase and stimulate its signaling function.
View Article and Find Full Text PDFCirc J
December 2018
Centro de Investigaciones Cardiovasculares, CONICET La Plata, Facultad de Ciencias Médicas, Universidad Nacional de La Plata.
Background: It has been shown that carvedilol and its non β-blocking analog, VK-II-86, inhibit spontaneous Ca release from the sarcoplasmic reticulum (SR). The aim of this study is to determine whether carvedilol and VK-II-86 suppress ouabain-induced arrhythmogenic Ca waves and apoptosis in cardiac myocytes.
Methods and results: Rat cardiac myocytes were exposed to toxic doses of ouabain (50 µmol/L).
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