Swelling-Induced K+ Fluxes in Vascular Smooth Muscle Cells are Mediated by Charybdotoxin-Sensitive K+ Channels

1 July 2001

journal article
research article
Published by S. Karger AG in Cellular Physiology and Biochemistry

Vol. 11 (6) , 295-310
https://doi.org/10.1159/000047816

Abstract

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 (IK_Ca), 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 IK_Ca expressed in erythrocytes. Their molecular origin and systems involved in the swelling-induced Ca²⁺_i-independent signal transduction pathway need further investigation.

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