Table 2.
Involvement of stretch-activated ion channels on biomechanical manifestations of myotubes.
| Effects of stretch on myotubes | involved ion channels | Activity of ion channels | Functional analysis | References |
|---|---|---|---|---|
| Increased amino acid uptake | Na pump | Increased Na pump activity | Inhibited by ouabain (depolarize the myotube's membrane potential) | Vandenburgh, 1983 |
| Increased amino acid uptake | Na pump | Not reported | Inhibited by ouabain and tetrodotoxin (inhibit sodium influx of an electrogenic nature) inhibit stretch-induced amino acid uptake, but not by amiloride (inhibit sodium influx of non-electrogenic nature) | Drummond et al., 2010 |
| Increased glucose transport | Na pump is not involved | Not reported | Not inhibited by tetrodotoxin | Johnston et al., 2011 |
| Increased glucose transport | Ca channel is not involved | Not reported | Not inhibited by reducing extracellular calcium level | Evans et al., 2019 |
| Increased protein synthesis | Na pump is not involved | Not reported | Not inhibited by tetrodotoxin | Clarke and Feeback, 1996 |
| Increased prostaglandins secretion | Na pump is not involved, but Ca channel might be | Not reported | Not inhibited by tetrodotoxin, but inhibited by reducing extracellular calcium level | De Deyne, 2000 |
| Increased prostaglandins secretion | Na pump is not involved | Not reported | Not inhibited by tetrodotoxin | Vandenburgh, 1982 |
| Increased acetylcholinesterase secretion | Na pump is not involved, but L-type Ca channel is involved | Not reported | Not inhibited by tetrodotoxin, but inhibited by nifedipine (L-type Ca channel inhibitor) | Tidball et al., 1998 |
| Increased damage of sarcoglycan deficient myotubes | L-type Ca channel is involved | Not reported | Inhibited by nifedipine and tranilast (inhibit growth factor-induced Ca influx) | Hubatsch and Jasmin, 1997 |
| Increased damage of sarcoglycan deficient myotubes | Stretch-activated cation channel (SAC) is involved | Increased SAC activity | Inhibited by Gadolinium chloride (GdCl3, stretch-activated channel inhibitor) | Tsivitse et al., 2005 |
| Increased damage of sarcoglycan deficient myotubes | Growth factor-regulated channel (GRC) is involved | Not reported | Inhibited by transfection with GRC antisense cDNA | Nguyen et al., 2005 |
| Increased damage of sarcoglycan deficient myotubes | Na+/H+ exchanger (NHE) and Na+/Ca2+ exchanger (NCX) are involved | Increased NHE activity | Inhibited by EIPA and cariporide (NHE inhibitors), and KBR (NCX inhibitor) | Juffer et al., 2014 |
| Activation of anabolical pathways (AKT, ERK, mTOR) | Volume-regulated anion channel (VRAC) is involved | Not reported | Inhibited by VRAC component LRRC8A ablation | Kumar et al., 2020 |