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.