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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary


CA2+ SIGNALLING IN CARDIAC TISSUE
Abstract number: O43

ONeill1 S., Sigalas1 C., Galfre1 E., Sitsapesan1 R.

Aims: 

The basis of Ca signalling in cardiac muscle is the sarcoplasmic reticulum (SR). This organelle releases Ca from its lumen into the cytoplasm of the cell via the Ca release channel it has within its membrane. This channel is also known as the ryanodine receptor (RyR). The activity of the RyR (its open probability: Po) is determined by the local concentration of Ca. In addition there are several accessory proteins that associate with the RyR to alter its Po.

Methods: 

We have examined one of these: Calmodulin. Recently it has been estimated that the free [CaM] is somewhere less than 100 nM1. We have used 50 nM to determine if this protein increases the Po of the RyR thereby increasing the frequency of spontaneous Ca releases that take place in the cell.

Results: 

Spontaneous sparks taking place in a single skinned ventricular myocyte isolated from a rat. Note that in Calmodulin (50 nM) the frequency of sparks is increased (7.2±0.5 to 9.4±1.1, n=3, p<0.05). Similar behaviour has been seen under Ca overloaded conditions when waves of Ca-induced Sa release (CICR) are increased in frequency from 8.7±1.3 min-1 to 12.7±2.0 (n=14; p<0.001).

Conclusion: 

As would be expected this increase of SR Ca release activity is associated with a decrease of the SR Ca content of about 30% and a reduction of wave amplitude.

1Wu X, Bers DM. Free and bound intracellular calmodulin measurements in cardiac myocytes. Cell Calcium 2007 April;41(4):353–64.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :O43

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