Regular ArticleChanges in Ultrastructural Calcium Distribution in Goat Atria During Atrial Fibrillation☆,☆☆
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Mechanism and Prevention of Atrial Remodeling and Their Related Genes in Cardiovascular Disorders
2023, Current Problems in CardiologyCitation Excerpt :Rapid depolarization of atrial myocytes during AF prolongs atrial systole, promotes calcium influx through calcium overload and leads to calcium release from sarcoplasmic reticulum calcium pool.26,27 Ausma et al.26 found that the content of muscle fiber membrane and mitochondrial membrane binding protein increased in the first 2 weeks of AF; the calcium content began to decrease at 4 weeks; At 16 weeks, the calcium content was close to or even lower than normal. It has been found that structural remodeling in AF is related to the hydrolysis of calcium activated proteins.
Different effects of norepinephrine and nerve growth factor on atrial fibrillation vulnerability
2019, Journal of CardiologyRedox control of cardiac remodeling in atrial fibrillation
2015, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :A consistent model of AngII and β1-adrenergic stimulated, protein kinase-dependent oxidative regulation of the cardiac Na+–K+ pump has been proposed, which indeed has important implications for cardiac physiology and disease, including AF [233]. Studies on atrial tissue have shown that an AF- or RAP-induced calcium-overload of cardiomyocytes induces ultrastructural alterations including morphologically altered mitochondria [20,21,28,234]. AF is associated with a higher demand of energy of cardiomyocytes resulting in transiently decreased concentrations of high energy phosphates and mitochondrial NADH [28,234].
Mechanisms of Arrhythmias and Conduction Disorders in Older Adults
2012, Clinics in Geriatric MedicineCitation Excerpt :These changes in electrophysiologic properties of the atrium, termed “electrical remodeling,” likely result from reduction in the L-type Ca2+ current and transient outward K+ current, a progressive late reduction in the density of voltage-gated Na+ channels, and gap junction redistribution that contributes to the slowing of conduction, thus increasing vulnerability of the atria to reentry and creating a condition in which AF perpetuates AF.79,102,106,107 These electrophysiologic changes are different from structural changes that are observed in patients with heart failure or in the senescent atria with gradual loss of myofibrils, myocyte hypertrophy, fragmentation of sarcoplasmic reticulum, and fibrosis with changes in the structure and shape of mitochondria.1,46,62,108–117 Changes in protein expression, similar to a de-differentiation process toward a partially fetal phenotype or that seen in hibernating myocardium, also take place with chronic AF.108,110
Increased Expression of Mineralocorticoid Receptor in Human Atrial Fibrillation and a Cellular Model of Atrial Fibrillation
2010, Journal of the American College of CardiologyCitation Excerpt :In our cellular AF model, intracellular calcium concentration was elevated by rapid depolarization (6). This result is similar to that found in a rapid-pacing model of AF (18). We also showed that intracellular calcium chelator BAPTA-AM and the L-type calcium-channel blocker verapamil abolished rapid depolarization-induced increment of MR expression.
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Please address all correspondence to: Dr J. Ausma, Dept of Physiology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: [email protected]
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This study was presented in part at the 71st Annual Scientific Sessions of the American Heart Association (Circulation Vol 98, I-683, 1998).