Myocytes cardiac

Several chemical compounds may cause inflammation or constriction of the blood vessel wall (vasoconstriction). Ergot alkaloids at high doses cause constriction and thickening of the vessel wall. Allylamine may also induce constriction of coronary arteries, thickening of their smooth muscle walls, and a disease state that corresponds to coronary heart disease. The culprit is a toxic reactive metabolite of allylamine, acrolein, that binds covalently to nucleophilic groups of proteins and nucleic acids in the cardiac myocytes. 

Zaccolo M, Pozzan T (2002) Discrete microdomains with high concentration of cAMP in stimulated rat neonatal cardiac myocytes. Science 295 1711-1715... 

Cardiac IKi is the major K+ current responsible for stabilizing the resting membranepotential and shaping the late phase of repolarization of the action potential in cardiac myocytes. The name should not be confused with that of an Intermediate conductance calcium-activated K+ channel, which sometimes is also called IK1. 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

PDE1C2 and PDE4A are expressed. PDE1C2 is found in the cilia of the epithelium, where it colocalizes with adenylyl cyclase. PDE4A is found throughout the epithelial layer, but not in cilia. Therefore, as in the kidney mesangial cells, different PDEs must be working on different cyclic nucleotide pools. More recently, substantial data has been developed for compartmenta-tion of cAMP and PDEs in cardiac myocytes. 

Kvl.5 In human atria, the Kvl.5 presents the ultrarapid delayed rectifier that contributes to the repolarization in the early phase of cardiac action potential. Selective blockers of Kvl.5 channels could be potentially beneficial in the treatment of atrial fibrillation because blocking Kvl. 5 could delay repolarization and prolong refractoriness selectively in cardiac myocytes. Examples for Kvl.5 blockers include AVE0118, S9947, and analogs of diphenyl phosphine oxide (DPO). 

Cardiac hypertrophy appears to be mediated by HS proteins (Izumo et al., 1988). Cardiac myocytes exposed to a hemodynamic stress have been found to increase their levels of heat shock proteins (Delcayre et al., 1988). Although experiments involving interference with HS protein synthesis were not done in these studies. 

Other drugs such as the neuroleptic, haloperidol, inhibit the induction of hsp70 mRNA in rodent neurons (Sharp et al.. 1992). Although this observation needs to be confirmed in the human population, it raises the possibility that an age-dependent defect in the production of HS proteins is exacerbated by a drug which is commonly used in demented elderly patients. The potential for certain pharmacologic agents to inhibit the HS response could increase the risk for untoward effects of atherosclerosis and hypoxia. A similar concern may be raised with certain calcium channel blockers which also have been found to reduce the synthesis of HS proteins in cardiac myocytes (Low-Friedrich and Schoeppe, 1991). 

Delcayre, C., Samuel, J.L., Marotte, F., Best, B.M., Mercadier, J.J., Rappaport, L. (1988). Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload. J. Clin. Invest. 82,460-468. 

Low-Friedrich, I. Schoeppe, W. (1991). Effects of calcium channel blockers on stress protein synthesis in cardiac myocytes. J. Cardiovasc. Pharmacol. 17,800-806. 

Deutsch J, Motlagh D, Russell B, and Desai TA. Fabrication of micro textured membranes for cardiac myocyte attachment and. orientation. J Biomed Mater Res, 2000, 53(3), 267-275. 

To certify the important role of Ca in the excitatory action of MTX, the effect of MTX on the Ca movements in cardiac muscle was examined at the cellular level. Figure 8 shows the time course of the Ca influx in the presence or absence of MTX (10 g/mL). The Ca uptake in the control experiment increased with time, to reach a saturation level about 5 min after administration of Ca. When MTX (10 g/mL) and Ca were applied simultaneously, the increase in Ca uptake at 5 min was 31% larger than that of the control. Furthermore, when the intracellular Ca concentration of isolated cardiac myocytes was determined from the Quin 2 fluorescence, MTX (10 g/mL) caused a marked increase in the free Ca concentration from 122 9 nM (control) to 380 23 nM, as shown in Figure 9. 

Figure 8. Effect of maitotoxin (MTX) on the time course of an increase in Ca uptake of cultured rat cardiac myocytes. Cbntrol ( ), and 10 g/mL MTX (o). Vertical lines indicate the standard error of mean (n=3). (Reproduced with permission from Ref. 20. Copyright 1987 Elsevier)...

The electrophysiological experiments reported here and done with patch-clamp techniques support this idea. The external application of MTX to isolated cardiac myocytes caused a sustained inward current which was carried by Ca . MTX did not increase the voltage-dependent Ca channel current, and both the time dependence and voltage dependence of the MTX-induced current were clearly different from those of the usual Ca channel current. These results suggest that the MTX-induced steady current is different from the usual voltage-dependent Ca channel current, and that this is possibly a current which flows through a new type of Ca -permeable channel. Tbe steady current described here may be responsible for the highly enhanced Ca influx induced by MTX and could account for the excitatory action of MTX on smooth and cardiac muscles. 

In order to understand the potential for haem proteins to mediate the oxidative modification of LDLs, the interaction between ruptured erythrocytes (Paganga et al., 1992) and ruptured myocytes (Bourne etal., 1994) with LDL has been explored. Previous studies from this group have demonstrated that ferryl myoglobin radicals and ruptured cardiac myocytes, which generate ferryl myoglobin species on activation (Turner et al., 1990,... 

Turner, J.J.O., Rice-Evans, C., Davies, M.J. and Newman, E.S.R. (1991). The formation of free radicals by cardiac myocytes under oxidative stress and the effects of electron-donating drugs. Biochem. J. 277, 833-837. 

Barry, W.H. and Bridge, J.H.B. (1993). Intracellular calcium homeostasis in cardiac myocytes. Circulation 87, 1806-1815. 

Bhatnagar, A., Srivastava, S.K. and Szabo, G. (1990). Oxidative stress alters specific membrane currents in isolated cardiac myocytes. Circ. Res. 67, 535-549. 

Coetzee, W.A. and Opie, L.Fl. (1992). Effects of oxygen free radicals on isolated cardiac myocytes from guinea-pig ventricle Electrophysiological studies. J. Mol. Cell. Cardiol. 24, 651-663. 

It has been proposed that NO mediates the myocardial depression associated with sepsis (F6, L14). NO synthesis induced by endotoxin blunts beta-adrenergic responsiveness (B2). In vivo, the use of NO synthase inhibitors led to conflicting results (M26), with a general decreased cardiac output and oxygen delivery being observed. NO synthase inhibition improved left ventricular contractility in endo-toxemic pigs but also increased ventricular afterloads, which ultimately is detrimental to cardiac function (H20). Possible sources of NO in the heart may be the vascular cells, the endothelial cells, and the cardiac myocytes (P6). 

B2. Balligand, J. L., Ungureanu, D Kelly, R. A., Kobzik, L., Pimental, D Michel, T and Smith, T. W., Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium. J. Clin. Invest. 91, 2314-2319(1993). 

Other plasminogen activator inhibitors are PAI-3, which is believed to be identical to the activated protein C inhibitor, and proteinase nexin 1, found in the renal epithelial cells, cytosol of fibroblasts, and cardiac myocytes (37, 42, 44, 45). 

Raff Cardiac myocytes are also very large. 

Burton PBJ, Raff MC, Kerr P, Yacoub MH, Barton PJR 1999 An intrinsic timer that controls cell-cycle withdrawal in cultured cardiac myocytes. Dev Biol 216 659—670 Chen X, Ko LJ, Jayaraman L, Prives C 1996 p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells. Genes Dev 10 2438—2451 Duesbery NS, Choi T, Brown KD et al 1997 CENP-E is an essential kinetochore motor in maturing oocytes and is masked during mos-dependent cell cycle arrest at metaphase II. Proc Natl Acad Sci USA 94 9165-9170... 

Resting cells do not express iNOS but the capacity to express this enzyme after specific stimuli is present in several tissues. Cells such as macrophages, endothelial cells, kidney cells, chondrocytes, cardiac myocytes, pancreatic islets and fibroblasts... 

Superoxide generation was detected via the NADPH-dependent SOD-inhibitable epinephrine oxidation and spin trapping [15,16], Grover and Piette [17] proposed that superoxide is produced equally by both FAD and FMN of cytochrome P-450 reductase. However, from comparison of the reduction potentials of FAD (-328 mV) and FMN (190 mV) one might expect FAD to be the most efficient superoxide producer. Recently, the importance of the microsomal cytochrome h558 reductase-catalyzed superoxide production has been shown in bovine cardiac myocytes [18]. 

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