Cardiac muscle cell

Another type of cardiomyopathy is termed dilated cardiomyopathy. Mutations in the genes encoding dystrophin, muscle LIM protein (so called because it was found to contain a cysteine-tich domain originally detected in three proteins Lin-II, Isl-1, and Mec-3), and the cyclic response-element binding ptotein (CREB) have been implicated in the causation of this condition. The first two proteins help organize the conttactile ap-params of cardiac muscle cells, and CREB is involved... 

Skeletal and cardiac muscles also have important differences. Skeletal muscle cells are elongated and run the length of the entire muscle furthermore, these cells have no electrical communication between them. Cardiac muscle cells, on the other hand, branch and interconnect with each other. Intercellular junctions found where adjoining cells meet end-to-end are referred to as intercalated discs. Two types of cell-to-cell junctions exist within these discs. Desmosomes hold the muscle cells together and provide the structural support needed when the heart beats and exerts a mechanical... 

Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles.

Garibaldi S, Brunelli C, Bavastrello V, Ghigliotti G, Nicolini C (2006) Carbon nanotube biocompatibility with cardiac muscle cells. Nanotechnology 17 391-397. 

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... 

Diltiazem reduces transmembrane influx of calcium ions into cardiac muscle cells and vascular smooth musculature. It causes widening of coronary and peripheral vessels. It increases coronary blood flow, thus, preventing the development of coronary artery spasms. It lowers elevated blood pressure and reduces tachycardia. 

Amlodipine shows a preference for binding vascular smooth muscle cells over cardiac muscle cells, thus acting as a peripheral arterial vasodilator (Pfizer, Inc. 2005). Like most other CCB dihydropyridines, amlodipine is highly protein bound and heavily metabolized. In contrast to felodipine, this compound is not influenced by grapefruit juice and appears to show fewer drug-drug interactions. 

The action of administered acetylcholine on effector systems innervated by parasympathetic postganglionic neurons (smooth muscle cells, cardiac muscle cells, and exocrine gland cells) resembled the actions produced by the naturally occurring plant alkaloid muscarine. The actions of both acetylcholine and muscarine on the visceral effectors are similar to those produced by parasympathetic nerve stimulation. Furthermore, the effects of acetylcholine, muscarine, and parasympathetic nerve stimulation on visceral effectors are antagonized by atropine, another plant alkaloid. 

Angiotensin II stimulates the influx of Ca" " into cardiac muscle cells and can exert a direct inotropic effect at cardiac muscle. In addition, angiotensin II can stimulate the sympathoadrenal system and thereby increase myocardial contractility. In contrast to its effects on vascular smooth muscle, the ability of angiotensin to increase the contractile force of the heart is far less potent. Therefore, in spite of the positive chronotropic and inotropic effects produced by angiotensin II, cardiac output is rarely increased. In fact, angiotensin II may decrease cardiac output through reflex bradycardia induced by the rise in peripheral resistance that it causes. In contrast, centrally administered angiotensin II increases both blood pressure and cardiac output. 

In some cell types (including cardiac muscle cells, pancreatic cells), another second messenger", the cyclic ADP-ribose (Fig. 6.8), is involved in opening the ryanodin receptors (Lee et al., 1994). The cADP-ribose is formed from NAD by an enzymatic pathway with the help of an ADP-ribosyl cyclase. 

Moore DH, Ruska H Electron microscope study of mammalian cardiac muscle cells. J Biophys Biochem Cytol 1957 3 261-267. 

Shibata Y, Miyahara A, Okayama T, Kuraoka A, Iida H Gap junction formation and regulation in cultured adult rat and guinea pig cardiac muscle cells in Kanno Y, Kataoka K, Shiba Y, Shibata Y Shimazu T (eds) Intercellular Communication through Gap Junctions. Progress in Cell Research, vol 4. Amsterdam, Elsevier, 1995, pp 151-154. 

Figure 7.53 The mechanism of action of digitoxin in cardiac muscle cells.

The calcium channel blockers currently used to treat angina pectoris are listed in Table 22-3. Although the chemistry and exact mechanism of action of each drug are somewhat distinct, all of these agents exert their effects by limiting calcium entry into specific cardiovascular tissues. Certain calcium channel blockers are said to be selective if they affect vascular smooth muscle, but have little or no affect on the heart. Nonselective calcium channel blockers affect the vasculature and inhibit calcium entry into cardiac muscle cells. Individual agents are discussed below. 

Because drugs like verapamil slow down the heart rate by inhibiting calcium entry into cardiac muscle cells, excessive bradycardia (less than 50 beats per minute) may occur in some patients receiving these drugs. Calcium channel blockers also limit calcium entry into vascular smooth muscle, which may cause peripheral... 

Thorburn A. 1994. Ras activity is required for phenylephrine-induced activation of mitogen-activated protein kinase in cardiac muscle cells. Biochem Biophys Res Commun 205 1417-1422. 

Iijima, Y., Laser, M., Shiraishi, H., Willey, C.D., Sundaravadivel, B., Xu, L., McDermott, P.J., and Kuppuswamy, D. 2002. c-Raf/MEK/ERK pathway controls protein kinase C-mediated p70S6K activation in adult cardiac muscle cells. J. Biol. Chem. 277 23065-23075. 

Zak, R. 1974. Development and proliferative capacity of cardiac muscle cells. Circ. Res. 34-35 (Suppl. II) 17—25. 

Depolarization of vascular smooth muscle activates the L-type calcium channels, which results in increased cytosolic concentrations of calcium and hence increased tone. Calcium channel blockers (e.g., verapamil and diltiazem) block the influx of calcium through the L-type voltage-dependent channels located on vascular smooth muscle and cardiac muscle cells as well as cardiac nodal cells. Therefore, they are used in the treatment of angina, hypertension, and certain arrhythmias. 

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