Stretch-activated calcium channels

Ypey DL, Weidema AF, Hold KM, Van der Laarse A, Ravesloot JH, Van Der Plas A, Nijweide PJ. 1992. Voltage, calcium, and stretch activated ionic channels and intracellular calcium in bone cells. J Bone Miner Res. 7 Suppl 2 S377-87. 

Finally, an increase in volume or pressure within a tube or hollow organ causes stretch or distortion of the smooth muscle in the organ wall. This may cause activation of stretch-activated Ca++ channels. The subsequent influx of calcium initiates contraction of the smooth muscle. This process is referred to as myogenic contraction and is common in blood vessels. 

Arteriolar resistance changes that take place in order to maintain a constant blood flow are explained by the myogenic mechanism. According to this mechanism, vascular smooth muscle contracts in response to stretch. For example, consider a situation in which blood pressure is increased. The increase in pressure causes an initial increase in blood flow to the tissue. However, the increased blood flow is associated with increased stretch of the vessel wall, which leads to the opening of stretch-activated calcium channels in the vascular smooth muscle. The ensuing increase in intracellular calcium results in vasoconstriction and a decrease in blood flow to the tissue toward normal. 

Diagram of the structures involved in the stretch reflex arc. I is an inhibitory interneuron E indicates an excitatory presynaptic terminal la is a primary intrafusal afferent fiber Ca2+ denotes activator calcium stored in the sarcoplasmic reticulum of skeletal muscle RyR channels indicates the Ca2+ release channels. 

A recent paper from Iwata et al. (2003) described a channel of the TRP family which is activated in response to growth factors or stretch, and whose activity is elevated in dystrophic skeletal and cardiac muscle. Under normal conditions, the GRC is located on vesicles in the cytoplasm, but translocates to the sarcolemma in response to growth factor signaling or stretch. This translocation is calcium-dependent, and, interestingly, requires a Gd3+-sensitive conductance, which could represent a basal level of GRC activity or some other perhaps MS-type channel. In addition, the translocation is inhibited by ruthenium red, a blocker of ryanodine receptor-dependent release of SR calcium, suggesting that store calcium release is also necessary for sarcolemmal GRC insertion. Whether the GRC is an SOC was not reported. 

Ko KS, Arora PD, McCulloch CA. Cadherins mediate intercellular mechanical signaling in fibroblasts by activation of stretch-sensitive calcium permeable channels. I Biol Chem. 2001 276 35967-35977. 

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