Ryanodine receptor/Ca2+ release channels and their regulation by endogenous effectors.

Abstract

Current evidence suggests that excitable and nonexcitable cells may contain one or both of two intracellular Ca2+ release channels. Release of Ca2+ from intramembrane compartments can be triggered by the binding of the second messenger inositol I ,4,5-trisphosphate (lP3) to the IP3 receptor/Ca2+ release channel (for review, see 6). It also can be mediated by the ryanodine receptor (RyR)/Ca2+ release channel in response to a surface membrane action potential and/or a change in the concentration of a second messenger, by a mechanism referred to in musele as excitation-contraction (E-C) coupling. In striated muscle, rapid release of Ca2+ from the intracellular compart­ ment, sarcoplasmic reticulum (SR), is initiated by a surface membrane action potential that is communicated to the SR at specialized areas where the junctional SR comes in close contact with the surface membrane or tubular infoldings of the surface membrane (T-tubule); at these areas large protein structures are present that span the gap between the two membrane systems. These structures have been termed feet (see C rranzini-Armstrong & A Jorgensen, this volume) and are now commonly known as ryanodine receptor/Ca2+ release channels because of the presence of an intrinsic ci+ channel activity within the feet structures, and their ability to bind the plant