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• W2116585504 startingPage "H1160" @default.
• W2116585504 abstract "The ventricular action potential (AP) is characterized by a fast depolarizing phase followed by a repolarization that displays a second upstroke known as phase 2. This phase is generally not present in mouse ventricular myocytes. Thus we performed colocalized electrophysiological and optical recordings of APs in Langendorff-perfused mouse hearts founding a noticeable phase 2. Ryanodine as well as nifedipine reduced phase 2. Our hypothesis is that a depolarizing current activated by Ca(2+) released from the sarcoplasmic reticulum (SR) rather than the electrogenicity of the L-type Ca(2+) current is crucial in the generation of mouse ventricular phase 2. When Na(+) was partially replaced by Li(+) in the extracellular perfusate or the organ was cooled down, phase 2 was reduced. These results suggest that the Na(+)/Ca(2+) exchanger functioning in the forward mode is driving the depolarizing current that defines phase 2. Phase 2 appears to be an intrinsic characteristic of single isolated myocytes and not an emergent property of the tissue. As in whole heart experiments, ventricular myocytes impaled with microelectrodes displayed a large phase 2 that significantly increases when temperature was raised from 22 to 37°C. We conclude that mouse ventricular APs display a phase 2; however, changes in Ca(2+) dynamics and thermodynamic parameters also diminish phase 2, mostly by impairing the Na(+)/Ca(2+) exchanger. In summary, these results provide important insights about the role of Ca(2+) release in AP ventricular repolarization under physiological and pathological conditions." @default.
• W2116585504 created "2016-06-24" @default.
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• W2116585504 creator A5038134144 @default.
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• W2116585504 date "2012-03-01" @default.
• W2116585504 modified "2023-10-06" @default.
• W2116585504 title "Intracellular Ca²⁺release underlies the development of phase 2 in mouse ventricular action potentials" @default.
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• W2116585504 doi "https://doi.org/10.1152/ajpheart.00524.2011" @default.
• W2116585504 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3311451" @default.
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