Swelling-Induced K+ Fluxes in Vascular Smooth Muscle Cells are Mediated by Charybdotoxin-Sensitive K+ Channels
| Parent link: | Cellular Physiology and Biochemistry.— , 1997- Vol. 11, iss. 6.— 2001.— [P. 295–310] |
|---|---|
| Other Authors: | , , , , , , |
| Summary: | Title screen This study examines the relative contributions of K-Cl cotransport and K+ channels to swelling-induced K+ fluxes in vascular smooth muscle cells (VSMC). DIOA known as a potent inhibitor of erythrocyte K-Cl cotransport exerts diverse side-effects on VSMC and can not be used to analyze the role of this carrier in swelling-induced K+ fluxes. Other inhibitors of K-Cl cotransport (furosemide, okadaic acid and calyculin A) did not affect K+ fluxes in VSMC triggered by swelling. Swelling-induced K+ fluxes in VSMC were also not affected by K+ channel blockers such as TEA, glibenclamide and apamin, but were blocked by Ba2+ and charybdotoxin (ChTX), a potent inhibitor of Ca2+- and voltage-gated K+ channels. Swelling-induced K+ influx in VSMC was diminished in Ca2+-free medium and in cells loaded with Ca2+ chelator BAPTA, but was not accompanied by detectable elevation of [Ca2+]i. In contrast to Ca2+-induced hyperpolarization of erythrocytes triggered by activation of intermediate conductance Ca2+-gated K+ channels (IKCa), neither clotrimazole nor calmodulin antagonists (R24571, trifluoroperazine, fluphenazine) affected swelling-induced K+ influx in VSMC. In conclusion, K+ fluxes triggered in swollen VSMC are mediated by Ba2+- and ChTX-sensitive K+ channels. These channels are distinct from IKCa expressed in erythrocytes. Their molecular origin and systems involved in the swelling-induced Ca2+i-independent signal transduction pathway need further investigation. |
| Published: |
2001
|
| Subjects: | |
| Online Access: | http://www.karger.com/Article/Abstract/47816 |
| Format: | Electronic Book Chapter |
| KOHA link: | https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=639222 |