DOI: 10.5061/dryad.70gk2
title: Data from: Cellular hypertrophy and increased susceptibility to spontaneous calcium-release of rat left atrial myocytes due to elevated afterload

description: 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&lt;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.
description: RyR_Sham-1Images of 18 atrial myocytes stained with anti RyR-2 antibody from hearts from Sham-operated ratsRyR_AoB-1Images of 18 atrial myocytes stained with anti-RyR-2 antibody from aortic banded ratsSham_controlLine scan images Ca transients in 12 fluo-3-AM loaded atrial myocytes from Sham-operated hearts stimulated at 1 Hz. Note: These are raw images; those presented in paper represent averages of consecutive transientsAoB_controlLine scan images of Ca transients from 8 fluo-3-AM loaded atrial myocytes from aortic banded rat hearts. Note: these are raw data of consecutive transients; transients presented in the paper represent averages of consecutive transientsSham di-8-ANEPPSZ-stacks of 20 di-8-ANEPPS-stained atrial myocytes from Sham operated rat heartsAoB di-8-ANEPPSZ-stacks of 13 di-8-ANEPPS-stained atrial myocytes from aortic banded rat heartsSham caffeine dataLine scan images of electrically stimulated and caffeine-induced Ca transients from 10 fluo-3-AM loaded atrial myocytes from Sham operated heartsAoB caffeine dataLine scan images of electrically stimulated and caffeine-induced Ca transients from 13 fluo-3-AM loaded atrial myocytes from aortic banded rat heartssham 4HzTxt data from 12 fluo-3-AM loaded atrial myocytes from Sham operated rat hearts subject to 4 Hz pacing followed by a period of at least 70 s without stimulationAoB HzTxt data from 13 fluo-3-AM loaded atrial myocytes from aortic banded hearts