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Modulation of Ca2+-dependent K+ transport by modifications of the NAD+/NADH ratio in intact human red cells
Affiliation:1. Division of Gastroenterology, Ospedale di Acireale, Azienda Sanitaria Provinciale di Catania, Catania, Italy;2. Department PROMISE, University of Palermo, Palermo, Italy;3. Medicine & Metabolic Diseases, Fondazione IRCCS Ca'' Granda, Ospedale Maggiore Policlinico, Milan, Italy;4. Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy;5. Department BIOMETEC, University of Catania, Catania, Italy;6. Deparment of Clinical and Molecular Medicine, University of Gothenburg, Sweden;7. Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy;1. Institut Clínic Cardiovascular (ICCV), Hospital Clínic, Universitat de Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain;2. Arrhythmias Unit, Hospital Sant Joan de Déu, University of Barcelona, Barcelona, Spain;3. Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain;4. Cardiovascular Genetics Center, Institut d''Investigació Biomèdica Girona (IDIBGI), University of Girona, Girona, Spain;5. Medical Science Department, School of Medicine, University of Girona, Girona, Spain;6. Cardiology Service, Hospital Josep Trueta, Girona, Spain
Abstract:The effects of variations of the NAD+/NADH quotient on the uptake of 86Rb by human red cells loaded by non-disruptive means with the chelator Benz2 and different amounts of 45Ca has been examined. The NAD+/NADH quotient was modified by the addition of pyruvate and/or lactate or xylitol. It was found that the uptake of 86Rb at a given intracellular Ca2+ concentration was faster in the reduced state (lactate or xylitol added). Metabolic changes were associated with variations of the redox state. However, glycolitic intermediates did not significantly modify the apparent affinity for Ca2+ of the Ca2+-dependent K+ channel in one-step inside-out vesicles prepared from the erythrocyte membrane. Taken together, these results suggest that modifications of the cytoplasmic redox potential could modulate the sensitivity to Ca2+ of the Ca2+-dependent K+ channel in the human red cells under physiological conditions. This conclusion is consistent with previous findings in inside-out vesicles of human erythrocytes using artificial electron donors.
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