Open AccessAge‐related changes in cellular electrophysiology and calcium handling for atrial fibrillation
Author(s) -
Xu GuoJun,
Gan TianYi,
Tang BaoPeng,
Chen ZuHeng,
Jiang Tao,
Song JianGuo,
Guo Xia,
Li Jinxin
Publication year - 2013
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12084
Subject(s) - phospholamban , atrial fibrillation , medicine , repolarization , electrophysiology , sinus rhythm , endocrinology , calcium , patch clamp , cardiology , calcium channel , diastole , fibrillation , l type calcium channel , ryanodine receptor , chemistry , biology , blood pressure
Abstract This study was to investigate whether or not the dysfunction of atrial repolarization and abnormality of the intracellular Ca 2+ handling protein was augmented with ageing. Four groups of dogs were studied, adult and aged dogs in sinus rhythm ( SR ) and atrial fibrillation ( AF ) induced by rapid atrial pacing. We used whole cell patch clamp recording techniques to measure L‐type Ca 2+ current in cardiomyocytes dispersed from the left atria. Expressions of the Ca 2+ handling protein were measured by real‐time quantitative reverse transcription‐polymerase chain reaction and Western blot methods. Cardiomyocytes from old atria showed longer action potential ( AP ) duration to 90% repolarization, lower AP plateau potential and peak L‐type Ca 2+ current densities at both age groups in SR . AF led to a higher maximum diastolic potential, an increase of amplitude of phase 0, decreases of AP duration to 90% repolarization, plateau potential and peak L‐type Ca 2+ current densities. Compared to the adult group, mRNA and protein expressions of the L‐type calcium channel a1c were decreased, whereas expressions of calcium adenosine triphosphatase were increased in the aged group. Compared to SR group, expressions of Ca 2+ handling protein except for phospholamban were significantly decreased in both age groups with AF . We conclude that these ageing‐induced electrophysiological and molecular changes showed that general pathophysiological adaptations might provide a substrate conducive to AF .