ArticleBMC research notes2026
Effect of VSOR/VRAC blocker tamoxifen on contractile activity of primary neonatal cardiomyocytes and isolated perfused heart.
Article in BMC research notes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
objectiveTamoxifen, a non-steroidal triphenylethylene antiestrogen, is a widely prescribed drug for treating and preventing estrogen receptor-positive breast cancer. The aim of this study was to evaluate the inotropic and chronotropic effects of tamoxifen on primary cultured neonatal cardiomyocytes and isolated adult Langendorff-perfused hearts.
resultsOsmotic swelling of primary cultured neonatal cardiomyocytes activated large anionic currents with the biophysical phenotype of the volume-sensitive outwardly rectifying (VSOR) chloride channel (also known as VRAC, volume-regulated anion channel). Tamoxifen at 10 µM suppressed VSOR/VRAC by ~ 84–85% in a voltage-independent manner. The same maneuver nearly stopped the spontaneous beating of the cardiomyocytes with no change in the contraction amplitude. In isolated Langendorff-perfused hearts, tamoxifen produced a significant negative chronotropic effect, as evidenced by a decrease in heart rate. No significant inotropic effect was observed, as there were no detectable changes in left ventricular systolic pressure, left ventricular developed pressure, and left ventricular end-diastolic pressure. At the single contraction level, administration of 10 µM tamoxifen resulted in broadening of the contraction amplitude histogram and a significant shift of the peak-to-peak interval histogram towards more prolonged values with signs of ectopic events.
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