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Sarcoplasmic reticulum functions

Sarcoplasmic reticulum function and contractile consequences in ureteric smooth muscles... [Pg.208]

Zderic SA, Rohrmann D, Gong C et al 1996 The decompensated detrusor II evidence for loss of sarcoplasmic reticulum function after bladder outlet obstruction in the rabbit. J Urol 156 587-592... [Pg.254]

Bouchard, R. A., and Bose, D. (1991). Influence of Experimental Diabetes on Sarcoplasmic Reticulum Function in Rat Ventricular Muscle. Am J Physiol 260(2 Pt 2) H341-54. [Pg.308]

Divet, A., and Huchet-Cadiou, C., 2002, Sarcoplasmic reticulum function in slow- and fast-twitch skeletal muscles from mdx mice, Pflugers Arch, 444, pp 634-643. [Pg.456]

Kukreja, R. C., A. B. Weaver, and M. L. Hess. 1989. Stimulated human neutrophils damage cardiac sarcoplasmic reticulum function by generation of oxidants. [Pg.96]

In the zone of Z membrane, invaginations of sarcolemma regularly occur, constituting the secondary system of T tubules or transversal, which is not connected to the sarcoplasmic reticulum. Functionally, these ones intervene by a trap system in the caption of Ca ions released during the muscle excitation and in metabolic exchanges of the fibrillar apparatus T tubules system conveys the excitation from the sarcolemma to the fibrillar apparatus, causing the fibres contraction, by releasing Ca. ... [Pg.369]

The trigger for all musele eontraetion is an increase in Ca eoneentration in the vicinity of the muscle fibers of skeletal muscle or the myocytes of cardiac and smooth muscle. In all these cases, this increase in Ca is due to the flow of Ca through calcium channels (Figure 17.24). A muscle contraction ends when the Ca concentration is reduced by specific calcium pumps (such as the SR Ca -ATPase, Chapter 10). The sarcoplasmic reticulum, t-tubule, and sarcolemmal membranes all contain Ca channels. As we shall see, the Ca channels of the SR function together with the t-tubules in a remarkable coupled process. [Pg.555]

Calsequestrin is the major calcium storage protein of the sarcoplasmic reticulum in skeletal and cardiac muscles. It is highly acidic and has a large capacity for Ca2+. Calsequestrin functions to localize calcium near the junctional face of the terminal cistemae from which calcium can be released into the cytosol via the ryanodine receptor. [Pg.314]

Sarcoplasmic reticulum (SR) is a form of the smoothfaced endoplasmic reticulum (ER) in muscles. It functions as an intracellular Ca2+ store for muscle contraction. Ca2+ is energetically sequestered into the SR by Ca2+-pump/sarcoplasmic endoplasmic reticulum Ca2+-ATPase (SERCA) and released via Ca2+ release channels on stimuli (ryanodine receptor in striated muscles and inositol 1,4,5-trisphosphate receptor in most smooth muscles). Endoplasmic reticulum in non-muscle tissues also functions as an intracellular Ca2+ store. [Pg.1110]

Pathogenesis of MH is not completely understood. Skeletal muscle, however, is the one tissue in MH with proven abnormalities, and it is further thought that the basic defect that causes the syndrome lies in the calcium regulation system found within the myoplasm. For example, calcium transport function appears to be decreased in the sarcoplasmic reticulum, mitochondria, and sarcolemma. Thus, the suggestion has been made that MH is characterized by a generalized membrane defeet. [Pg.402]

TBT and TFT are membrane-active molecules, and their mechanism of action appears to be strongly dependent on organotin(IV) lipophilicity. They function as ionophores and produce hemolysis, release Ca(II) from sarcoplasmic reticulum, alter phosphatodylseiine-induced histamine release, alter mitochondrial membrane permeability and perturb membrane enzymes. Organotin(IV) compounds have been shown to affect cell signaling they activate protein kinase and increase free arachidonic acid through the activation of phospholipase... [Pg.420]

The number of different proteins in a membrane varies from less than a dozen in the sarcoplasmic reticulum to over 100 in the plasma membrane. Most membrane proteins can be separated from one another using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), a technique that has revolutionized their study. In the absence of SDS, few membrane proteins would remain soluble during electrophoresis. Proteins are the major functional molecules of membranes and consist of enzymes, pumps and channels, structural components, antigens (eg, for histocompatibility), and receptors for various molecules. Because every membrane possesses a different complement of proteins, there is no such thing as a typical membrane structure. The enzymatic properties of several different membranes are shown in Table 41-2. [Pg.419]

Purified membrane proteins or enzymes can be incorporated into these vesicles in order to assess what factors (eg, specific lipids or ancillary proteins) the proteins require to reconstitute their function. Investigations of purified proteins, eg, the Ca " ATPase of the sarcoplasmic reticulum, have in certain cases suggested that only a single protein and a single lipid are required to reconstitute an ion pump. [Pg.421]

Most living cells, including muscle, maintain the cytoplasmic Ca concentration at submicromolar levels, against steep gradients of [Ca ], both at the cell surface and across the endoplasmic reticulum membrane [17]. In the musele cell two membrane systems are primarily involved in this function the sarcoplasmic reticulum and the surface membrane. [Pg.57]

Spatial relationships between functional sites in the sarcoplasmic reticulum Ca -ATPase... [Pg.98]

Blasie, J.K., Herbette, L., Pierce, D.H., Pascolini, D., Skita, V., Scarpa, A. and Fleischer, S. (1985) In Structure and Function of Sarcoplasmic Reticulum, Symposium on Structure and Function of Sarcoplasmic Reticulum, Kobe, Japan, November 1-4, 1982 (Fleischer, S. and Tonomura, Y., Eds.), pp. 51-62, Academic Press, Orlando. [Pg.110]

Reactive oxygen species modify the structure and function of the cardiac sarcoplasmic reticulum calcium release channel. Cardioscience 2, 19-25. [Pg.71]

Shattock, M.J., Matsuura, H. and Hearse, D.J. (1991). Functional and electrophysiolc cal effects of oxidant stress on isolated ventricular muscle role for oscillatory calcium release from sarcoplasmic reticulum in arrhythmogenesis. Cardiovasc. Res. 25, 645-651. [Pg.72]

Explain the functions of the following myosin crossbridges, troponin, tropomyosin, sarcomeres, Z lines, neuromuscular junction, transverse tubules, and sarcoplasmic reticulum... [Pg.139]

Turner WH, Brading AF 1997 Smooth muscle of the bladder in the normal and the diseased state pathophysiology, diagnosis and treatment. Pharmacol Ther 75 77—110 van Breemen C, Chen Q, Laher I 1995 Superficial buffer barrier function of smooth muscle sarcoplasmic reticulum. Trends Pharmacol Sci 16 98-105 Wray S 1993 Uterine contraction and physiological mechanisms of modulation. Am J Physiol 264 C1-C18... [Pg.5]

Missiaen L, Taylor CW, Berridge MJ 1992 Luminal Ca2+ promoting spontaneous Ca2+ release from inositol trisphosphate-sensitive stores in rat hepatocytes. J Physiol 455 623-640 Nazer MA, van Breemen C 1998 Functional linkage of Na+-Ca2+ exchange and sarcoplasmic reticulum Ca2+ release mediates Ca2+ cycling in vascular smooth muscle. Cell Calcium 24 275-283... [Pg.40]

Blaustein MP, Golovina VA, Song H et al 2002 Organization of Ca2+ stores in vascular smooth muscle functional implications. In Role of the sarcoplasmic reticulum in smooth muscle. Wiley, Chichester (Novartis Found Symp 246) p 125-141 Karaki H, Ozaki H, Hori M et al 1997 Calcium movements, distribution and function in smooth muscle. Pharmacol Rev 49 157-230... [Pg.47]

The sarcoplasmic reticulum and smooth muscle function evidence from transgenic mice... [Pg.228]

Arii T, Ohyanagi M, Shibuya J, Iwasaki T 1999 Increased function of the voltage-dependent calcium channels, without increase of Ca2+ release from the sarcoplasmic reticulum in the arterioles of spontaneous hypertensive rats. Am J Hypertens 12 1236-1242 Attree O, Olivos IM, Okabe I et al 1992 The Lowe s oculocerebrorenal syndrome gene encodes a protein highly homologous to inositol polyphosphate-5-phosphatase. Nature 358 239-242 Brading AF, Turner WH 1994 The unstable bladder towards a common mechanism. Br J Urol 73 3-8... [Pg.252]


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See also in sourсe #XX -- [ Pg.155 ]




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