Action Potential Prolongation, β-Adrenergic Stimulation, and Angiotensin II as Co-factors in Sarcoplasmic Reticulum Instability.

ABSTRACT: Introduction: Increases in action potential duration (APD), genetic or acquired, and arrhythmias are often associated; nonetheless, the relationship between the two phenomena is inconstant, suggesting coexisting factors. β-adrenergic activation increases sarcoplasmic reticulum (SR) Ca2+-content; angiotensin II (ATII) may increase cytosolic Ca2+ and ROS production, all actions stimulating RyRs opening. Here we test how APD interacts with β-adrenergic and AT-receptor stimulation in facilitating spontaneous Ca2+ release events (SCR). Methods: Under "action potential (AP) clamp", guinea-pig cardiomyocytes (CMs) were driven with long (200 ms), normal (150 ms), and short (100 ms) AP waveforms at a CL of 500 ms; in a subset of CMs, all the 3 waveforms could be tested within the same cell. SCR wer

SUBMITTER: Ronchi C 

PROVIDER: S-EPMC6333690 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature