Channel stretch-activated

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. 

Kannan MS, Prakash YS, Brenner T, Mickelson JR, Sieck GC 1997 Role of ryanodine receptor channels in Ca2+ oscillations of porcine tracheal smooth muscle. Am J Physiol 272 L659-L664 Kirber MT, Walsh JVJ, Singer JJ 1988 Stretch-activated ion channels in smooth muscle a mechanism for the initiation of stretch-induced contraction. Pfliig Arch Eur J Physiol 412 339-345... 

Wellner MC, Isenberg G 1993 Stretch-activated nonselective cation channels in urinary bladder myocytes importance for pacemaker potentials and myogenic response. Exper Suppl (Basel) 66 93-99... 

Somlyo Can we relate the kinetics of this process to what happens in whole muscle As you know, when a smooth muscle is stretched and there is a myogenic contraction, there is a lag phase of about a second. This is surprisingly long for channel activation. How can you relate these kinetics to the kinetics of a lag of 500 ms Stretch activation has also been suggested to involve PLC activation. 

Brading Do your expression cells generate sparks Do you get spontaneous release from the SR in these cells You showed some of these cells where the SR was overloaded with Ca2+, and I wondered whether there is a difference in the behaviour of the SR depending on the amount of intracellular Ca2+. This is going back to this business of stretch-activated channels and whether if you stretch the SR by superfilling it with Ca2+ and getting some osmotic expansion it changes its behaviour. 

Ca2+ is the major second messenger in the activation of smooth muscle contraction. Thus smooth muscle Ca2+ handling is of major importance to understanding its function. Ca2+ homeostasis is a balance of Ca2+ influx and extrusion. Influx is generally through channels, such as I, or T type Ca2+ channels or the so-called capacitive entry pathway, through stretch activated channels, leak pathways and reversed mode Na+/Ca2+ exchanger, which may... 

Mechanosensitive ion channels can be looked at as membrane-embedded mechano-electrical switches. They play a critical role in transducing physical stresses at the cell membrane (e.g. lipid bilayer deformations) into an electrochemical response. Two types of stretch-activated channels have been reported the mechanosensitive channels of large conductance (MscL) and mechanosensitive channels of small conductance (MscS). 

Homologs of VR1 with a high threshold (> 52°C) for activation by noxious heat, or sensitivity to membrane stretch, provisionally termed vanilloid receptor-like protein (VRL-1) (Caterina et al., 1999) and stretch-inactivated channel (SIC) (Suzuki et al., 1999), respectively, have been identified. Neither channel is activated by vanilloid agonists (Caterina et al., 1999 Suzuki et al., 1999). A mouse ortholog of VRL-1 acts as a growth factor regulated channel (GRC) permeable to Ca2+ ions (Kanzaki et al., 1999). A splice variant of VR1 (VR.5 sv) that lacks the majority of the intracellular N-terminal domain is refractory to activation by vanilloid agonists, protons or noxious... 

Stretch-activated MS channels are observed in a number of types of cells, including skeletal muscle. Original studies from Lansman and colleagues showed that a lower-activity, stretch-activated channel is present in both control and mdx muscle, with greater open probability in mdx myotubes and collagenase-isolated fibers (Franco... 

Franco-Obregon and Lansman, 1994) several other properties are also different, including increased activity with depolarization in Lansman (and other studies of canonical MS channels) but decreased activity with depolarization in Vandebrouck. Finally, McBride and Hamill (1992) observed stretch-activated channels with no clear evidence for stretch-inactivated channels in dystrophic muscle, although the number of channels studied might not have been sufficient to observe such channels. 

Gu, C.X., Juranka, P.F., and Morris, C.E., 2001, Stretch-activation and stretch-inactivation of Shaker-IR, a voltage-gated K+ channel, Biophys J, 80, pp 2678-2693. 

Maroto, R., Raso, A., Wood, T.G., Kurosky, A., Martinac, B., and Hamill, O.P., 2005, TRPC1 forms the stretch-activated cation channel in vertebrate cells, Nat Cell Biol, 7, pp 179-185. 

McBride, T.A., Stockert, B.W., Gorin, F.A., and Carlsen, R.C., 2000, Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions, J Appl Physiol, 88, pp 91-101. 

Davidson RM. 1993. Membrane stretch activates a high-conductance K+ channel in G292 osteoblastic-like cells. J Membr Biol 131 81-92. 

Duncan R, Misler S. 1989. Voltage-activated and stretch-activated Ba2+ conducting channels in an osteoblast-like cell line (UMR 106). FEBS Lett 251 17-21. 

Kizer N, Guo XL, Hruska K. 1997. Reconstitution of stretch-activated cation channels by expression of the alpha-subunit of the epithelial sodium channel cloned from osteoblasts. Proc Natl Acad Sci USA. 94 1013-8. 

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. 

Different mechanisms are involved in the opening of volume-regulatory ion channels they are cell type-dependent and involve direct channel activation by membrane stretch, alterations in intracellular free [Ca2+] or activation of membrane-bound signaling systems. For example, swelling of hepatocytes apparently opens stretch-activated nonselective cation channels, which allow passage of Ca2+into the cell (Bear, 1990). Swelling in turn stimulates phospholipase C to produce inositol-1,4,5-trisphosphate, which in turn mobilizes Ca2+ from intracellular stores. The resulting increase in [Ca2+] may then activate Ca2+-sensitive K+ channels, thus... 

Sackin, H. (1987). Stretch-activated potassium channels in renal proximal tubule. Am. J. Physiol. 253, F1253-1262. 

Recently, it has been demonstrated that mechanical stress rapidly induced phosphorylation of PDGF receptor, activation of integrin receptor, stretch-activation of cation channels, and production of G proteins. Once mechanical stress was sensed, protein kinase C and MAPKs were activated, leading to increased c-fos and c-Jun gene expression and enhanced transcription factor AP-1 DNA binding activity. The application of physical forces also rapidly resulted in expression of MAPK phosphatase-1 (MKP-1), which inactivates MAPKs. 

Davis MJ, Donovitz JA, Hood JD. Stretch-activated single-channel whole cell currents in vascular smooth muscle cells. Am J Physiol. 1992 262 0083-0088. 

Kirber MT, Walsh JV Jr, Singer JJ. Stretch-activated ion channels in smooth muscle A mechanism for the initiation of stretch-induced contraction. Pflugers Arch. 1988 412 339-345. 

Two different types of membrane-based osmosensors have been proposed for animal cells extracellular solute sensors and membrane stretch-activated sensors. The former sensors are conjectured to function by detecting changes in the concentration of specific ions, for instance, sodium ion, in the external fluids. There is some indirect evidence for sodium-specific sensors in animal cells, and sodium-gated cation channels have been proposed as candidates for this role. However, no direct evidence for their involvement as upstream osmoregulatory elements has yet been presented. 

Stretch-activated proteins in animal cell membranes that are candidates for osmosensing activity include mechanosensitive ion channels and the membrane-localized enzyme phospholipase A2 (PLA2). The former proteins remain to be conclusively linked to osmosensing. Activity of PLA2 is sensitive to packing of the lipid bilayer of the cell and is responsive to osmotic changes, two attributes that mark it as a prime candidate for a stretch-activated sensor (Lehtonen and Kinnunen, 1995). 

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