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Calcium effectors

contractions without fusion requires both the fast generation and fast removal of Ca2 . In order to respond to such rapid fluctuations, the on- and off-rates of Ca2 binding to troponin C must also be high.

Smooth muscle contraction

Compared with skeletal and cardiac muscle, smooth muscle contraction is a slow process. The enormous variability that exists between different smooth muscle cells makes it difficult to draw general conclusions concerning their signalling mechanisms. In smooth muscle there is no troponin. Contraction is achieved through the phosphorylation of the P chain of myosin by MLCK and this is activated by Ca2 -calmodulin. (Note: calmodulin-dependent

kinase also phosphorylates MLCK in skeletal muscle but here it does not cause contraction. Instead, it appears to affect the force of contraction.)

Some smooth muscle cells in arteries and veins display a mechanism similar to that in the heart, where entry of calcium through VOCCs is further amplified by Ca2 -induced Ca2 release from internal stores.47–49 In contrast to cardiac cells, however, these smooth muscle cells operate a low gain mechanism so that the entry of external calcium contributes a larger proportion of the global calcium signal.

In addition to depolarization-dependent mechanisms, many smooth muscle cells are also activated by receptors that activate PLC, forming IP3 and releasing Ca2 from internal stores.50 Calcium signals are generated by both IP3Rs and RyRs and there are indications that these two release channels might cooperate with each other in some types of smooth muscle.

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