Excitation-contraction coupling cardiac cells

Babiychuk EB, Draeger A 2000 Annexins in cell membrane dynamics. Ca2+-regulated association of lipid microdomains. J Cell Biol 150 1113-1124 Ber DM 2001 Excitation-contraction coupling and cardiac contractile force, 2nd edn. Kluwer Academic Publishers, Dordrecht/Boston/London Blaustein MP, Golovina VA 2001 Structural complexity and functional diversity of endoplasmic reticulum Ca2+ stores. Trends Neurosci 24 602—608 Flynn ER, Bradley KN, Muir TC, McCarron JG 2001 Functionally separate intracellular Ca2+ stores in smooth muscle. J Biol Chem 276 36411-36418 Fry CH, WuCl 997 Initiation of contraction in detrusor smooth muscle. Scand J Urol Nephrol Suppl 184 7-14... 

Cardiac muscle is highly dependent on calcium influx for normal function. Impulse generation in the sinoatrial node and conduction in the atrioventricular node—so-called slow-response, or calcium-dependent, action potentials—may be reduced or blocked by all of the calcium channel blockers. Excitation-contraction coupling in all cardiac cells requires calcium influx, so these drugs reduce cardiac contractility in a dose-dependent fashion. In some cases, cardiac output may also decrease. This reduction in cardiac mechanical function is another mechanism by which the calcium channel blockers can reduce the oxygen requirement in patients with angina. 

Although it is believed that the primary defect in early heart failure resides in the excitation-contraction coupling machinery of the heart, the clinical condition also involves many other processes and organs, including the baroreceptor reflex, the sympathetic nervous system, the kidneys, angiotensin II and other peptides, and death of cardiac cells. Recognition of these factors has resulted in evolution of a variety of treatment strategies (Table 13-1). 

Cav 1.2 L-type CClC cardiac muscle, endocrine cells excitation-contraction coupling, hormone secretion DHPs lethal... 

Kockskamper, J., Ahmmed, G.U., Zima, A.V, Sheehan, K.A., Glitsch, H.G., and Blatter, L. A. 2004. Palytoxin disrupts cardiac excitation-contraction coupling through interactions with P-type ion pumps. Am J Physiol Cell Physiol 287, C527-538. 

The maintenance of physiologic calcium concentrations in the intracellular and extracellular spaces is vital for the preservation and function of cell membranes propagation of neuromuscular activity regulation of endocrine and exocrine secretory functions blood coagulation cascade platelet adhesion process bone metabolism muscle cell excitation/contraction coupling and mediation of the elec-trophysiologic slow-channel response in cardiac and smooth-muscle tissue. 

Cardiac Muscle. Calcium inhibitory agents may interfere with excitation-contraction coupling processes in myocardial or vascular smooth muscle cells by a number of mechanisms including l) inhibition of the slow inward current through direct competition for slow channels or interference with the membrane binding of Ca2+ 2) interference with the release... 

Functional expression of chimeras of the skeletal and cardiac muscle Uj subunit in skeletal muscle cells from mdg mice showed that the cytoplasmic loop between repeats II and III determines the type of excitation-contraction coupling (Fig. 2). The loop from the skeletal muscle calcium channel Ujs supports contraction in the absence of calcium influx, whereas the loop from the cardiac calcium channel Ujc subunit induces contraction only in the presence of calcium influx (Tanabe etal., 1990). These results suggest that the loop between repeats II and III interacts with the ryanodine receptor in a tissue-specific manner. 

The excitation-contraction coupling processes of smooth muscle cells employ both extra- and intracellular sources of Ca +. As in skeletal and cardiac muscle cells, the intracellular source of Ca + is the sarcoplasmic reticulum. Although RyRs are the major pathway for Ca + release in striated muscle (Fleischer and Inui,... 

Triadins, a multiprotein family with different distribution of the various splice variants within the sarcoplasmic reticulum (SR). Their function may include involvement in excitation-contraction coupling, in triad targeting, in structural function, or in muscle differentiation. Triadin, a glycoprotein (Mr 95 kDa) expressed in both skeletal and cardiac muscle, was first identified in rabbit skeletal muscle involved in calcium release for muscle contraction. Recently, it has been reported that triadins are not triad-specific proteins. Two new skeletal muscle triadins may be involved in the architecture of the SR [I. Marty, Cell. Mol. Life Sci. 2004, 61, 1850 S. VassHopoulos etal, J. Biol. Chem. 2005, 280, 28601]. 

L-type calcium channels are the primary trigger for excitation-contraction (EC) coupling in cardiac, skeletal, and smooth muscles (Bean, 1989). They are also found in most central and peripheral neurons where they in part control calcium-dependent gene expression, as well as in endocrine cells and many types of non-excitable cells where they contribute to a variety of processes including exocytotic release. Unlike most synapses in the brain and spinal cord that rely on P/Q- and N-type calcium channels for neurotransmitter release, (Wheeler et al., 1994), the presynaptic terminals in photoreceptor cells rely on the Cav1.4 (a1F) L-type calcium channel for mediating glutamate release (Tachibana et al., 1993 Nachman-Clewner et al., 1999). Photoreceptor neurotransmission is atypical first,... 

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