Another long title. The whole thing is below.
This 8-page article quantifies in great detail the ATP sensitivity of ATP-regulated potassium channels, often referred to as IK(ATP). As the article shows by many references, it’s known that the epicardium of the heart is more sensitive to lack of oxygen (and therefore metabolic energy in the form of adenosine triphosophate — ATP) than then endocardium of the heart. The authors of this study first measured currents from ATP-regulated potassium channels in the presence of CN– (cyanide, which blocks the generation of ATP), and then more directly pulled off patches of cell membrane with ATP-regulated potassium channels, and tested them in the presence of varying concentrations of ATP. In both cases, action potentials (the way in which cardiac cells ‘fire’ to initiate contraction and signal each other) were shortened more in the epicardial patches than in those from the endocardium. The degree to which this shortening occurred and at what concentrations is well-documented in the article.
The results of this study are clear, well-presented, and extremely useful in modeling ischemia in the heart. It’s a long read, with a ton of experimental detail, but the results are worth slogging through all of that. This fundamental article on ATP-regulated potassium channels is a must-read for anyone wanting to study ischemia and infarction in the heart.