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Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle

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Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle. / Hübner, Christian A; Schroeder, Björn C; Ehmke, Heimo.

In: PFLUG ARCH EUR J PHY, Vol. 467, No. 3, 03.2015, p. 605-14.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hübner, CA, Schroeder, BC & Ehmke, H 2015, 'Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle', PFLUG ARCH EUR J PHY, vol. 467, no. 3, pp. 605-14. https://doi.org/10.1007/s00424-014-1684-y

APA

Hübner, C. A., Schroeder, B. C., & Ehmke, H. (2015). Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle. PFLUG ARCH EUR J PHY, 467(3), 605-14. https://doi.org/10.1007/s00424-014-1684-y

Vancouver

Hübner CA, Schroeder BC, Ehmke H. Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle. PFLUG ARCH EUR J PHY. 2015 Mar;467(3):605-14. https://doi.org/10.1007/s00424-014-1684-y

Bibtex

@article{12679b45a4154672abb2bc207f7293d5,
title = "Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle",
abstract = "Recent studies suggest that primary changes in vascular resistance can cause sustained changes in arterial blood pressure. In this review, we summarize current knowledge about Cl(-) homeostasis in vascular smooth muscle cells. Within vascular smooth muscle cells, Cl(-) is accumulated above the electrochemical equilibrium, causing Cl(-) efflux, membrane depolarization, and increased contractile force when Cl(-) channels are opened. At least two different transport mechanisms contribute to raise [Cl(-)] i in vascular smooth muscle cells, anion exchange, and cation-chloride cotransport. Recent work suggests that TMEM16A-associated Ca(2+)-activated Cl(-) currents mediate Cl(-) efflux in vascular smooth muscle cells leading to vasoconstriction. Additional proteins associated with Cl(-) flux in vascular smooth muscle are bestrophins, which modulate vasomotion, the volume-activated LRRC8, and the cystic fibrosis transmembrane conductance regulator (CFTR). Cl(-) transporters and Cl(-) channels in vascular smooth muscle cells (VSMCs) significantly contribute to the physiological regulation of vascular tone and arterial blood pressure.",
keywords = "Animals, Blood Pressure, Chloride Channels, Chlorides, Humans, Ion Transport, Muscle, Smooth, Vascular, Vasoconstriction",
author = "H{\"u}bner, {Christian A} and Schroeder, {Bj{\"o}rn C} and Heimo Ehmke",
year = "2015",
month = mar,
doi = "10.1007/s00424-014-1684-y",
language = "English",
volume = "467",
pages = "605--14",
journal = "PFLUG ARCH EUR J PHY",
issn = "0031-6768",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle

AU - Hübner, Christian A

AU - Schroeder, Björn C

AU - Ehmke, Heimo

PY - 2015/3

Y1 - 2015/3

N2 - Recent studies suggest that primary changes in vascular resistance can cause sustained changes in arterial blood pressure. In this review, we summarize current knowledge about Cl(-) homeostasis in vascular smooth muscle cells. Within vascular smooth muscle cells, Cl(-) is accumulated above the electrochemical equilibrium, causing Cl(-) efflux, membrane depolarization, and increased contractile force when Cl(-) channels are opened. At least two different transport mechanisms contribute to raise [Cl(-)] i in vascular smooth muscle cells, anion exchange, and cation-chloride cotransport. Recent work suggests that TMEM16A-associated Ca(2+)-activated Cl(-) currents mediate Cl(-) efflux in vascular smooth muscle cells leading to vasoconstriction. Additional proteins associated with Cl(-) flux in vascular smooth muscle are bestrophins, which modulate vasomotion, the volume-activated LRRC8, and the cystic fibrosis transmembrane conductance regulator (CFTR). Cl(-) transporters and Cl(-) channels in vascular smooth muscle cells (VSMCs) significantly contribute to the physiological regulation of vascular tone and arterial blood pressure.

AB - Recent studies suggest that primary changes in vascular resistance can cause sustained changes in arterial blood pressure. In this review, we summarize current knowledge about Cl(-) homeostasis in vascular smooth muscle cells. Within vascular smooth muscle cells, Cl(-) is accumulated above the electrochemical equilibrium, causing Cl(-) efflux, membrane depolarization, and increased contractile force when Cl(-) channels are opened. At least two different transport mechanisms contribute to raise [Cl(-)] i in vascular smooth muscle cells, anion exchange, and cation-chloride cotransport. Recent work suggests that TMEM16A-associated Ca(2+)-activated Cl(-) currents mediate Cl(-) efflux in vascular smooth muscle cells leading to vasoconstriction. Additional proteins associated with Cl(-) flux in vascular smooth muscle are bestrophins, which modulate vasomotion, the volume-activated LRRC8, and the cystic fibrosis transmembrane conductance regulator (CFTR). Cl(-) transporters and Cl(-) channels in vascular smooth muscle cells (VSMCs) significantly contribute to the physiological regulation of vascular tone and arterial blood pressure.

KW - Animals

KW - Blood Pressure

KW - Chloride Channels

KW - Chlorides

KW - Humans

KW - Ion Transport

KW - Muscle, Smooth, Vascular

KW - Vasoconstriction

U2 - 10.1007/s00424-014-1684-y

DO - 10.1007/s00424-014-1684-y

M3 - SCORING: Journal article

C2 - 25588975

VL - 467

SP - 605

EP - 614

JO - PFLUG ARCH EUR J PHY

JF - PFLUG ARCH EUR J PHY

SN - 0031-6768

IS - 3

ER -