Mechanism of calcium release from skeletal sarcoplasmic reticulum

1982 ◽  
Vol 66 (1) ◽  
pp. 193-201 ◽  
Author(s):  
Hiroshi Miyamoto ◽  
Efraim Racker
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release

scholarly journals Cardiac Sarcoplasmic Reticulum Calcium Release and Load Are Enhanced by Subcellular cAMP Elevations in PI3Kγ-Deficient Mice

2005 ◽  
Vol 96 (10) ◽  
pp. 1079-1086 ◽  
Author(s):  
Benoit-Gilles Kerfant ◽  
Dominica Gidrewicz ◽  
Hui Sun ◽  
Gavin Y. Oudit ◽  
Josef M. Penninger ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Sarcoplasmic Reticulum Calcium ◽  
Deficient Mice

scholarly journals Spontaneous calcium release in tissue from the failing canine heart

2009 ◽  
Vol 297 (4) ◽  
pp. H1235-H1242 ◽  
Author(s):  
Gregory S. Hoeker ◽  
Rodolphe P. Katra ◽  
Lance D. Wilson ◽  
Bradley N. Plummer ◽  
Kenneth R. Laurita
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Tissue Level ◽  
Calcium Handling ◽  
Canine Heart ◽  
Myocardial Cells ◽  
Spontaneous Release ◽  
Adrenergic Stimulation ◽  
Electrical Instability ◽  
Delayed Afterdepolarization

Abnormalities in calcium handling have been implicated as a significant source of electrical instability in heart failure (HF). While these abnormalities have been investigated extensively in isolated myocytes, how they manifest at the tissue level and trigger arrhythmias is not clear. We hypothesize that in HF, triggered activity (TA) is due to spontaneous calcium release from the sarcoplasmic reticulum that occurs in an aggregate of myocardial cells (an SRC) and that peak SCR amplitude is what determines whether TA will occur. Calcium and voltage optical mapping was performed in ventricular wedge preparations from canines with and without tachycardia-induced HF. In HF, steady-state calcium transients have reduced amplitude [135 vs. 170 ratiometric units (RU), P < 0.05] and increased duration (252 vs. 229 s, P < 0.05) compared with those of normal. Under control conditions and during β-adrenergic stimulation, TA was more frequent in HF (53% and 93%, respectively) compared with normal (0% and 55%, respectively, P < 0.025). The mechanism of arrhythmias was SCRs, leading to delayed afterdepolarization-mediated triggered beats. Interestingly, the rate of SCR rise was greater for events that triggered a beat (0.41 RU/ms) compared with those that did not (0.18 RU/ms, P < 0.001). In contrast, there was no difference in SCR amplitude between the two groups. In conclusion, TA in HF tissue is associated with abnormal calcium regulation and mediated by the spontaneous release of calcium from the sarcoplasmic reticulum in aggregates of myocardial cells (i.e., an SCR), but importantly, it is the rate of SCR rise rather than amplitude that was associated with TA.

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