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8 results for “atrial myocytes”
Data from: Cellular hypertrophy and increased susceptibility to spontaneous calcium-release of rat left atrial myocytes due to elevated afterload
Atrial remodeling due to elevated arterial pressure predisposes the heart to atrial fibrillation (AF). Although abnormal sarcoplasmic reticulum (SR) function has been associated with AF, there is little information on the effects of elevated afterload on atrial Ca2+-handling. We investigated the effects of ascending aortic banding (AoB) on Ca2+-handling in rat isolated atrial myocytes in comparison to age-matched sham-operated animals (Sham). Myocytes were either labelled for ryanodine receptor (RyR) or loaded with fluo-3-AM and imaged by confocal microscopy. AoB myocytes were hypertrophied in comparison to Sham controls (P<0.0001). RyR labeling was localized to the z-lines and to the cell edge. There were no differences between AoB and Sham in the intensity or pattern of RyR-staining. In both AoB and Sham, electrical stimulation evoked robust SR Ca2+-release at the cell edge whereas Ca2+ transients at the cell center were much smaller. Western blotting showed a decreased L-type Ca channel expression but no significant changes in RyR or RyR phosphorylation or in expression of Na+/Ca2+ exchanger, SR Ca2+ ATPase or phospholamban. Mathematical modeling indicated that [Ca2+]i transients at the cell center were accounted for by simple centripetal diffusion of Ca2+ released at the cell edge. In contrast, caffeine (10 mM) induced Ca2+ release was uniform across the cell. The caffeine-induced transient was smaller in AoB than in Sham, suggesting a reduced SR Ca2+-load in hypertrophied cells. There were no significant differences between AoB and Sham cells in the rate of Ca2+ extrusion during recovery of electrically-stimulated or caffeine-induced transients. The incidence and frequency of spontaneous Ca2+-transients following rapid-pacing (4 Hz) was greater in AoB than in Sham myocytes. In conclusion, elevated afterload causes cellular hypertrophy and remodeling of atrial SR Ca2+-release.
Ultrastructure of Atrial Myocytes in Patients in Sinus Rhythm and With Atrial Fibrillation
ClinicalTrials.gov study NCT01493128. IPD Sharing: Not stated. Countries: 0. Publications: 1.
Data from: Cellular hypertrophy and increased susceptibility to spontaneous calcium-release of rat left atrial myocytes due to elevated afterload
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Exploring Regulatory Mechanisms of Atrial Myocyte Hypertrophy of Mitral Regurgitation through Gene Expression Profiling Analysis: Role of NFAT in Cardiac Hypertrophy
GEO Series GSE63045. Homo sapiens. 10 samples. Type: Expression profiling by array.
Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy
GEO Series GSE17294. Homo sapiens. 11 samples. Type: Expression profiling by array.
Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy: left ventricle DCM
GEO Series GSE17530. Homo sapiens. 3 samples. Type: Expression profiling by array.
Atrial myocytes-derived exosomal microRNA contributes to atrial fibrosis in atrial fibrillation
GEO Series GSE210894. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
Transcriptional profile of rapidly stimulated atrial myocytes: Conservation with human atrial fibrillation
GEO Series GSE10598. Mus musculus. 4 samples. Type: Expression profiling by array.
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OpenNeuro
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