1. Calcium-release channels (ryanodine receptors) of canine cardiac sarcoplasmic reticulum (SR) were incorporated into lipid bilayer membranes at the tip of a patch pipette. Using (KD, 360 ,UM). On the return of pCa from 3 to > 8, the channels briefly re-opened. In the mammalian ventricular muscle, most of the Discussion). Studies on single cardiac SR Ca2+-release activator Ca2+ derives from the sarcoplasmic reticulum (SR) channels incorporated into planar lipid bilayers did not by Ca2+-induced Ca2+ release (CICR; for review see Fabiato, confirm the idea that Ca2+-dependent inactivation 1983;Wier, 1990 Meissner, 1986;Williams, 1992; Gybrke & Fill, 1993; see skinned cardiac cells suggested that gradation of CICR in Discussion). To explain the discrepancy it was suggested both rate and the amplitude of trigger [Ca2+] is the that the reconstituted Ca2+-release channels had not been consequence of both Ca2+ activation and Ca2+ inactivation exposed to the fast increase in [Ca2+] as it occurs in vivo of the SR Ca2P-release channels (Fabiato, 1985; see also (Fabiato, 1992).
Mitochondrial calcium content changes during each individual contraction cycle; a substantial amount of calcium is taken up during the systole and released during later systole and diastole.
Cardiac muscle contraction is triggered by a small and brief Ca2+ entry across the t-tubular membranes, which is believed to be locally amplified by release of Ca2+ from the adjacent junctional sarcoplasmic reticulum (SR)
Increased Thy-1 expression in GO orbital tissues and cultures is likely a consequence of the orbital disease process, reflecting both the presence of increased numbers of Thy-1-positive cells and higher expression on those cells. Adipogenesis itself does not appear to impact Thy-1 expression. Increased expression of this protein in GO could represent an adaptive response to cell injury, in effect limiting disease progression within the orbital adipose/connective tissues.
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