Figure 2
From: Myocardial contractility in the echo lab: molecular, cellular and pathophysiological basis
Molecular basis of contractility in normal heart. Crucial features are entry of Ca2+ ions through the voltage-sensitive L-type Ca2+ channels in response to the wave of depolarization, acting as a trigger for the release of Ca2+ ions from the sarcoplasmic reticulum (SR). The crux of the contractile process lies in the changing concentrations of Ca2+ ions in the myocardial cytosol. The varying actin-myosin overlap is shown for systole, when calcium ions arrive, and diastole, when calcium ions leave. At the end of systole, calcium stops interaction with troponin C and calcium ions are taken up into the SR by the activity of the pump called SERCA. Calcium taken up into the SR by the calcium uptake pump is stored within the SR before further release. The small amount of calcium that has entered the cell leaves predominantly through a Na+/Ca2+ exchanger. (Modified from Opie LH. Normal and abnormal cardiac function. Chapter 14, page 443. In Braunwald Zipes Libby Heart disease, 6th edition, W. B Saunders Company, 2001)