Fig. 2
From: Regulation of myocardial contraction as revealed by intracellular Ca2+ measurements using aequorin
Modified from Fig. 2 of [38] in an open access article published by Springer Nature with permission.
Schematic illustration showing the intracellular structure of a cardiac myocyte. The influx of Ca2+ from the interstitial fluid upon excitation causes the release of Ca2+ from the sarcoplasmic reticulum (SR). The released Ca2+ binds to troponin on thin filaments and triggers sarcomeric contraction (as in Fig. 1). Relaxation occurs as a result of uptake of Ca2+ by the SR Ca2+ pump, by extrusion of intracellular Ca2+ by Na+-Ca2+ exchangers, and partially by the sarcolemmal Ca2+ pump. It still remains elusive whether mitochondria play a significant role in Ca2+ handling under physiological conditions. The T-tubules and Z-lines run in parallel, causing Ca2+ sparks at/near the Z-lines. Thick and thin filaments, and titin are shown in the sarcomere (for simplicity, two titin molecules per half thick filament are shown). Troponin and tropomyosin exist on thin filaments, regulating actomyosin interaction in a [Ca2+]i-dependent manner (as in Fig. 1). LTCC, L-type Ca2+ channel; RyR, ryanodine receptor; PMCA, plasma membrane Ca2+ ATPase; NCX, Na+-Ca2+ exchanger; NHE, sodium-hydrogen exchanger.