Ventricular myocyte cells

Figure 4.5 Influence of oxidant stress on action potentials recorded In an isolated rabbit ventricular myocyte, (a) Control action potential, (b) Action potential recorded 3 min after exposure to oxidant stress induced by the photoactivation of rose bengal (50 nu). (c) Spontaneous and repetitive action potential discharges induced 6.5 min after exposure to rose bengal. Action potentials were recorded via a 2.5 MQ suction electrode and a current-clamp amplifier. The cell was stimulated at 0.1 Hz with a 2 ms suprathreshold current pulse and, when the cell showed automaticity (after 6 min), stimulation was stopped. Redrawn from Matsuura and Shattock (1991b).

Figure 4.7 Changes in intraceiiuiar calcium in cultured rat ventricular myocytes exposed to oxidant stress. Calcium was measured using the fluorescent probe Fura>2. The ratio of the Fura-2 fluorescence measured at 340 and 380 nm excitation is shown and this is proportional to the intracellular calcium concentration. The fast-speed traces shown (note the 3.5 s time-scale) were recorded after various durations of oxidant stress. Myocytes under control conditions (before t = 0) show spontaneous calcium transients. These transients decreased in frequency with oxidant stress until cells failed to show spontaneous activity but continued to maintain a low intracellular calcium.

The effect of cellular GSH depletion on /wa/K has also been studied using this model. Guinea-pig ventricular myocytes prepared from DEM-treated animals have been used to determine the effect of glutathione depletion on /xa/K- Myocytes prepared from DEM-treated animals showed a similar profile of glutathione content modification to that previously described in experiments using sarcolemmal homogenates. GSH levels in DEM-treated were reduced from a control value of 0.2 0.04 to 0.02 0.01 nmol/1 X10 cells. Jni/k at 0 mV was reduced from a control value of 1.1 0.12 to... 

Burton, K.P., Morris, A.C., Massey, K.D., Buja, L.M. and Hagler, H.K. (1990). Free radicals alterionic calcium levels and membrane phospholipids in cultured rat ventricular myocytes. J. Mol. Cell. Cardiol. 22, 1035-1047 (abstract). 

Shattock M. J. and Matsuura, H. (1993). Measurement of Na -K pump current in isolated rabbit ventricular myocytes using the whole-cell voltage-clamp technique. Inhibition of the pump by oxidant stress. Circ. Res. 72, 91-101. 

Quercetin and rutin suppressed photosensitized hemolysis of human erythrocytes with ho values equal to 40 p.mol l-1 and 150 jjlmt>I I 1, respectively [139]. Suppression of photohemolysis was accompanied by inhibition of lipid peroxidation. Morin inhibited oxygen radical-mediated damage induced by superoxide or peroxyl radicals to the human cells in the cardiovascular system, erythrocytes, ventricular myocytes, and saphenous vein endothelial cells [140]. Rutin protected against hemoglobin oxidation inside erythrocytes stimulated by prooxidant primaquine [141],... 

FIG. 3. Tight coupling in cardiac but not smooth muscle myocytes. Cells dialysed with 17 nM mobile Ca2+ buffer (EGTA). When depolarized, brief Ca2+ release events are seen in ventricular myocytes, indicating RyR gating occurs before the mobile buffer can scavenge the gating Ca2+ ions. Conversely, in smooth muscle cells CICR is completely blocked. The simplest interpretation of these data is that Ca2+ ions must traverse a distance of at least lOOnm, the distance beyond which the mobile buffer can prevent a rise in Ca2+. (From Collier et al 2000.)... 

In vitro Disaggregated cells Repolarizing currents (e.g., IKs, IK1, Ito), depolarizing currents (e.g., INa) currents, ICa (whole cell patch-clamp) Disaggregated cells ventricular myocytes mouse atrial tumor cells (AT-1) immortalized cardiac muscle cells (HL-1) Jost et al.,-65 Liu and Antzelevitch 66 Jurkiewicz and Sanguinetti 67 Li et al. 68 Yang and Roden 69 Banyasz et al. 70 Xia et al.71... 

Morley GE, Anumonwo JMB, Delmar M Effects of 2,4-dinitrophenol or low [ATP on cell excitability and action potential propagation in guinea pig ventricular myocytes. Circ Res 1992 71 821-830. 

Lindner, M., Erdmann, E., and Beuckelmann, D.J., 1998, Calcium content of the sarcoplasmic reticulum in isolated ventricular myocytes from patients with terminal heart failure. J Mol Cell Cardiol, 30(4), pp 743-9. 

Apart from HCN channels, genistein (42) also acted on other types of channels present in cardiac cells. Chiang et al. [306] examined the impact of this isoflavone on the L-type calcium and cAMP- dependent chloride currents in guinea pig ventricular myocytes. Using the voltage-clamp technique they found that genistein (42) reversibly inhibited L-type calcium currents in a dose-dependent manner. Surprisingly daidzein (40), which was ineffective with respect to many other channel types, also decreased L-type calcium currents in myocytes. Opposite to calcium currents, the cAMP-dependent... 

Woodley SL, Ikenouchi H, Barry WH (1991) Lysophosphatidylcholine increases cytosolic calcium in ventricular myocytes by direct action on the sarcolemma. J Mol Cell Cardiol 23 671-80... 

A muscle cell (freshly isolated mouse ventricular myocyte) was retained at a 5-pm constriction in a PDMS-glass chip. Extracellular potential recordings were measured during the spontaneous contraction of the muscle cell. Experiments were usually performed within 3 h after cell isolation in order to maintain cell viability [270]. 

Karliner JS, Kagiya T, Simpson PC. 1990. Effects of pertussis toxin on alpha 1-agonist-mediated phosphatidylinositide turnover and myocardial cell hypertrophy I neonatal rat ventricular myocytes. Experientia (Basel) 46 81-84. 

Fig. 8.3 Effects of dietary selenium on p-adrenergic responses in rat heart, (a) L-type Ca2+ currents (I(a i recorded from ventricular myocytes with depolarization from —70mV to OmV, for 200 ms. Mean ( SEM) values of peak amplitudes of IcaL in both experimental and control groups. The cell capacitances of these three groups of cardiomyocytes were similar, (b) Average current-voltage relationships for peak IcaL (measured as the difference between the peak Ca2+ current and the end of 200-ms depolarization). The maximums of IcaL of both experimental groups were shifted to the right with respect to the control, (c) The threshold potentials were significantly more negative and activation potentials were more positive in both experimental groups with respect to the control. (Adapted from Sayar et al. 2000.)...

Shubieta, H.E., McDonough, PM., Harris, A.N., Knowlton, K.U., Glembotski, C.C., Brown, J.H., and Chien, K.R. 1990. Endothelin induction of inositol phosphate hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy. J.Biol. Chem. 265 20555-20562. 

Leptin has been shown to increase hyperplasia of the murine atrial HL-1 cell line as well as pediatric cardiomyocytes (Tajmir et al. 2004). Activation of ERK and phosphatidylinositol 3-kinase was demonstrated and implicated in the increase in cell number. It should be noted that leptin-induced hypertrophy has also been shown in human pediatric ventricular myocytes which was associated with increased ERK, p38, and JAK phosphorylation (Madani et al. 2006). 

The results from studies using the HL-1 cell line are difficult to compare to primary culture of ventricular myocytes since the two models would likely respond to stimuli differently in view of the fact that the primary response of HL-1 cells is hyperplasia, not hypertrophy. 

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