Ca2 Sensitivity

Ca2+ is the central factor in myocardial contraction and the potential of a cardiac system to be activated by Ca2+ is characterized by its Ca2+ sensitivity. Originally, Ca2+ sensitivity was used to define the relationship between Ca2+ concentration and tension, but later the relationship was extended from tension to other parameters as well, e.g. myofibrillar ATPase activity or fluorescence intensity. Conventionally, Ca2+ sensitivity is illustrated by plotting the pCa against the selected parameter, expressed as percentage of the control value (Fig. H6).

The pCa curve can shift to the left "increased Ca2+ sensitivity" or to the right "decreased Ca2+ sensitivity". The extent of shift can be estimated from the difference of the pCa values at 50% activity. The shift may be small, 0.05 pCa, or large >1.0 pCa.

There are several factors, which influence the Ca2+ sensitivity of the myocardium. In case of the Force - pCa relationship the factors are:TN-I phosphorylation, p-tropomyosin, aging, acidosis, sarcomere length, temperature, ionic strength, caffeine, or other agents (Bers, 2001). It should be mentioned that most Force - pCa relationship were measured on cardiac myofilaments with their sarcolemma removed by Triton treatment, "skinned fibres"; the Ca2+ sensitivity of the skinned preparations may differ from those of intact heart ventricles.

Some authors attribute the differences in Ca2+ sensitivity among hearts of various animals, frog, guinea pig, rat, rabbit, or cow, to differences in their TN-C content. On the other hand, others feel that the Ca2+ sensitivity is not based on the single reaction between Ca2+ and TN-C but it rather reflects a series of reactions involved in the signal transduction initiated by Ca2+.

The level of intracellular Ca2+ plays a major role in the Ca2+ activation of the myofilament. Fig. H7 shows the factors establishing the Ca2+ level. Ca2+ enters the myoplasm through the Ca channels, it may trigger release of new Ca2+ from the SR or it may be stored in the SR. The intracellular Ca2+ can initiate contraction through the TN system. Excess Ca2+ is leaving the heart cell through the sarcolemma.

Fig. H7. Regulation of Ca + activation of the myofilament. (Courtesy of Dr. Helen Rarick)

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