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, Jahrgang 467, Nr. 3, 03.2015, S. 605-14.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -