| First Author | Ulyanova AV | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 4 | Pages | e0194980 |
| PubMed ID | 29694371 | Mgi Jnum | J:261954 |
| Mgi Id | MGI:6154814 | Doi | 10.1371/journal.pone.0194980 |
| Citation | Ulyanova AV, et al. (2018) Voltage-dependent inward currents in smooth muscle cells of skeletal muscle arterioles. PLoS One 13(4):e0194980 |
| abstractText | Voltage-dependent inward currents responsible for the depolarizing phase of action potentials were characterized in smooth muscle cells of 4th order arterioles in mouse skeletal muscle. Currents through L-type Ca2+ channels were expected to be dominant; however, action potentials were not eliminated in nominally Ca2+-free bathing solution or by addition of L-type Ca2+ channel blocker nifedipine (10 muM). Instead, Na+ channel blocker tetrodotoxin (TTX, 1 muM) reduced the maximal velocity of the upstroke at low, but not at normal (2 mM), Ca2+ in the bath. The magnitude of TTX-sensitive currents recorded with 140 mM Na+ was about 20 pA/pF. TTX-sensitive currents decreased five-fold when Ca2+ increased from 2 to 10 mM. The currents reduced three-fold in the presence of 10 mM caffeine, but remained unaltered by 1 mM of isobutylmethylxanthine (IBMX). In addition to L-type Ca2+ currents (15 pA/pF in 20 mM Ca2+), we also found Ca2+ currents that are resistant to 10 muM nifedipine (5 pA/pF in 20 mM Ca2+). Based on their biophysical properties, these Ca2+ currents are likely to be through voltage-gated T-type Ca2+ channels. Our results suggest that Na+ and at least two types (T- and L-) of Ca2+ voltage-gated channels contribute to depolarization of smooth muscle cells in skeletal muscle arterioles. Voltage-gated Na+ channels appear to be under a tight control by Ca2+ signaling. |
