%0 Journal Article
%T Ryanodine receptors
%A E Michelle Capes
%A Randall Loaiza
%A H¨Śctor H Valdivia
%J Skeletal Muscle
%D 2011
%I BioMed Central
%R 10.1186/2044-5040-1-18
%X In striated and smooth muscle cells, fluctuations in the intracellular levels of Ca2+ ions greatly determine the magnitude and duration of contractile force. In cardiac and skeletal muscle, depolarization of the external membrane and its invaginations, the T-tubules, elicits swift and massive Ca2+ release from the sarcoplasmic reticulum (SR), which in turn causes 'flooding' of the contractile myofilaments with Ca2+ and induction of contraction. This exquisitely coordinated series of events, in which an electrical stimulus (depolarization) is converted into a mechanical contraction, is collectively termed 'excitation-contraction (EC) coupling', and it has as central players the voltage-dependent Ca2+ channels/dihydropyridine receptors (DHPRs) as the sarcolemmal voltage sensors, and the Ca2+ release channels/ryanodine receptors (RyRs) as the SR Ca2+ release conduits. The structural and functional communication between the voltage sensor and the RyR dictate the magnitude of Ca2+ release from the SR, and thus the force of contraction. In fact, genetic mutations in either of these two proteins, or alterations in the environment that promotes their functional coupling, are known to cause ventricular arrhythmias, hypercontractures and/or pathological remodeling of cellular structures. Excellent reviews on DHPRs have appeared recently [1,2]. In the current review, we focus on RyRs to discuss their most prominent structural and functional attributes, and to suggest mechanisms by which their dysfunction leads to disease.RyRs are not restricted to striated muscle. This class of intracellular Ca2+ release channels is also found in the endoplasmic reticulum of neurons, exocrine cells, smooth-muscle cells, epithelial cells, lymphocytes, sea-urchin eggs, and many others [3]. In all of these cells, RyRs play a central role in the regulation of the intracellular free Ca2+ concentration ([Ca2+]i), whose elevation triggers a cascade of events that culminates in, for example, neurotran
%U http://www.skeletalmusclejournal.com/content/1/1/18