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Does sarcoplasmic reticulum inhibition modulate the stretch-induced prolongation of action potentials in rat atrial myocytes?
Does sarcoplasmic reticulum inhibition modulate the stretch-induced prolongation of action potentials in rat atrial myocytes?
Sarcoplasmic reticulum function and intracellular calcium balance play an important role in modulating the shape of rat atrial action potentials during stretch.
SR calcium handling modulates stretch effects on rat atrial APD; leaves open translation to human arrhythmias or therapies.
We have investigated the role of sarcoplasmic reticulum (SR) in the modulation on rat action potentials by stretch. The action potentials were recorded intracellularly from rat atrial myocytes in an isolated atrial preparation with small, physiological stretch produced by pressure (1-3 mmHg) inside the atria. The SR function was inhibited by pharmacological interventions, either with ryanodine (100 nmol L-1), thapsigargin (10 nmol L-1) or caffeine (1 mmol L-1). The duration of action potentials was increased by stretch from 1 to 3 mmHg. The repolarization indices APD30% (P < 0.05), APD60% (P < 0.01), and APD90% (P < 0.01) were all increased significantly (n=10). Ryanodine, thapsigargin, and caffeine inhibited this prolongation, or even reversed the effect with repolarization indices APD30% (P < 0.05) and APD60% (P < 0.05) which decreased in stretch with thapsigargin treatment. As a conclusion, we suggest that the SR and the intracellular calcium balance play an important role in the modulation of the shape of the rat atrial action potential during stretch.
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Han et al. (1999) studied this question.
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