PHYS SHORTS: Activation of small conductance Ca2+-activated K+ channels suppresses Ca2+ transient скачать в хорошем качестве

PHYS SHORTS: Activation of small conductance Ca2+-activated K+ channels suppresses Ca2+ transient

In this Physiology Shorts video Giedrius Kanaporis (Department of Physiology & Biophysics, Rush University Medical Center, Chicago, Illinois, USA) talks about their study 'Activation of small conductance Ca2+-activated K+ channels suppresses Ca2+ transient and action potential alternans in ventricular myocytes'. Read more in The Journal of Physiology: 'Activation of small conductance Ca2+-activated K+ channels suppresses Ca2+ transient and action potential alternans in ventricular myocytes.' Giedrius Kanaporis et al. 601(1), pp. 51-67 https://physoc.onlinelibrary.wiley.co... Transcript: Hi I am Giedrius Kanaporis from Rush University in Chicago. I am a member of Dr. Blatter’s research group investigating different aspects of calcium handling in cardiac myocytes. Today, I am pleased to give you a short presentation of our recent study. We investigated the possible role of small conductance Ca activated potassium channels in cardiac arrhythmogenesis. The physiological role of SK channels in the heart is poorly understood and the block of these channels in ventricular myocytes have only a minor effect on action potential duration. However, to our surprise, activation of SK channels in rabbit ventricular myocytes resulted in a significant shortening of action potential, suggesting that ventricular myocytes express functional SK channels. The beat-to beat alternation in intracellular calcium release and action potential durations is called cardiac alternans. Alternans is a well-established risk factor and contributes to the development of cardiac arrhythmias. Here we demonstrated that activation of SK channel suppresses both calcium and APD alternans. We simulated long QT conditions in ventricular cells by blocking to different potassium channels. As expected, action potential prolongation increased degree of alternans which was successfully suppressed by subsequential activation of SK channels. Based on these observations we suggest that SK channel activation could serve as potential therapeutic intervention to prevent development of alternans and arrhythmias in patients with Long QT syndrome. Thank you for taking time to learn more about our study. It was selected as an Editor’s choice and the full paper was published in Volume 601, Issue 1 in The Journal of Physiology. Please contact me at [email protected], if you have any questions. Thank you.