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Disruption of vascular Ca2+-activated chloride currents lowers blood pressure

Standard

Disruption of vascular Ca2+-activated chloride currents lowers blood pressure. / Heinze, Christoph; Seniuk, Anika; Sokolov, Maxim V; Huebner, Antje K; Klementowicz, Agnieszka E; Szijártó, István A; Schleifenbaum, Johanna; Vitzthum, Helga; Gollasch, Maik; Ehmke, Heimo; Schroeder, Björn C; Hübner, Christian A.

in: J CLIN INVEST, Jahrgang 124, Nr. 2, 03.02.2014, S. 675-86.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Heinze, C, Seniuk, A, Sokolov, MV, Huebner, AK, Klementowicz, AE, Szijártó, IA, Schleifenbaum, J, Vitzthum, H, Gollasch, M, Ehmke, H, Schroeder, BC & Hübner, CA 2014, 'Disruption of vascular Ca2+-activated chloride currents lowers blood pressure', J CLIN INVEST, Jg. 124, Nr. 2, S. 675-86. https://doi.org/10.1172/JCI70025

APA

Heinze, C., Seniuk, A., Sokolov, M. V., Huebner, A. K., Klementowicz, A. E., Szijártó, I. A., Schleifenbaum, J., Vitzthum, H., Gollasch, M., Ehmke, H., Schroeder, B. C., & Hübner, C. A. (2014). Disruption of vascular Ca2+-activated chloride currents lowers blood pressure. J CLIN INVEST, 124(2), 675-86. https://doi.org/10.1172/JCI70025

Vancouver

Heinze C, Seniuk A, Sokolov MV, Huebner AK, Klementowicz AE, Szijártó IA et al. Disruption of vascular Ca2+-activated chloride currents lowers blood pressure. J CLIN INVEST. 2014 Feb 3;124(2):675-86. https://doi.org/10.1172/JCI70025

Bibtex

@article{00d091d5f9e14bb18180a82d2a91ae8f,
title = "Disruption of vascular Ca2+-activated chloride currents lowers blood pressure",
abstract = "High blood pressure is the leading risk factor for death worldwide. One of the hallmarks is a rise of peripheral vascular resistance, which largely depends on arteriole tone. Ca2+-activated chloride currents (CaCCs) in vascular smooth muscle cells (VSMCs) are candidates for increasing vascular contractility. We analyzed the vascular tree and identified substantial CaCCs in VSMCs of the aorta and carotid arteries. CaCCs were small or absent in VSMCs of medium-sized vessels such as mesenteric arteries and larger retinal arterioles. In small vessels of the retina, brain, and skeletal muscle, where contractile intermediate cells or pericytes gradually replace VSMCs, CaCCs were particularly large. Targeted disruption of the calcium-activated chloride channel TMEM16A, also known as ANO1, in VSMCs, intermediate cells, and pericytes eliminated CaCCs in all vessels studied. Mice lacking vascular TMEM16A had lower systemic blood pressure and a decreased hypertensive response following vasoconstrictor treatment. There was no difference in contractility of medium-sized mesenteric arteries; however, responsiveness of the aorta and small retinal arterioles to the vasoconstriction-inducing drug U46619 was reduced. TMEM16A also was required for peripheral blood vessel contractility, as the response to U46619 was attenuated in isolated perfused hind limbs from mutant mice. Out data suggest that TMEM16A plays a general role in arteriolar and capillary blood flow and is a promising target for the treatment of hypertension.",
keywords = "15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid, Animals, Arterioles, Blood Pressure, Brain, Chloride Channels, Cloning, Molecular, DNA, Complementary, Electrophysiology, Estrogen Antagonists, HEK293 Cells, Humans, Hypertension, Membrane Potentials, Mesenteric Arteries, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle, Smooth, Vascular, Neoplasm Proteins, Pericytes, Retina, Tamoxifen, Time Factors, Vascular Resistance, Vasoconstrictor Agents",
author = "Christoph Heinze and Anika Seniuk and Sokolov, {Maxim V} and Huebner, {Antje K} and Klementowicz, {Agnieszka E} and Szij{\'a}rt{\'o}, {Istv{\'a}n A} and Johanna Schleifenbaum and Helga Vitzthum and Maik Gollasch and Heimo Ehmke and Schroeder, {Bj{\"o}rn C} and H{\"u}bner, {Christian A}",
year = "2014",
month = feb,
day = "3",
doi = "10.1172/JCI70025",
language = "English",
volume = "124",
pages = "675--86",
journal = "J CLIN INVEST",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "2",

}

RIS

TY - JOUR

T1 - Disruption of vascular Ca2+-activated chloride currents lowers blood pressure

AU - Heinze, Christoph

AU - Seniuk, Anika

AU - Sokolov, Maxim V

AU - Huebner, Antje K

AU - Klementowicz, Agnieszka E

AU - Szijártó, István A

AU - Schleifenbaum, Johanna

AU - Vitzthum, Helga

AU - Gollasch, Maik

AU - Ehmke, Heimo

AU - Schroeder, Björn C

AU - Hübner, Christian A

PY - 2014/2/3

Y1 - 2014/2/3

N2 - High blood pressure is the leading risk factor for death worldwide. One of the hallmarks is a rise of peripheral vascular resistance, which largely depends on arteriole tone. Ca2+-activated chloride currents (CaCCs) in vascular smooth muscle cells (VSMCs) are candidates for increasing vascular contractility. We analyzed the vascular tree and identified substantial CaCCs in VSMCs of the aorta and carotid arteries. CaCCs were small or absent in VSMCs of medium-sized vessels such as mesenteric arteries and larger retinal arterioles. In small vessels of the retina, brain, and skeletal muscle, where contractile intermediate cells or pericytes gradually replace VSMCs, CaCCs were particularly large. Targeted disruption of the calcium-activated chloride channel TMEM16A, also known as ANO1, in VSMCs, intermediate cells, and pericytes eliminated CaCCs in all vessels studied. Mice lacking vascular TMEM16A had lower systemic blood pressure and a decreased hypertensive response following vasoconstrictor treatment. There was no difference in contractility of medium-sized mesenteric arteries; however, responsiveness of the aorta and small retinal arterioles to the vasoconstriction-inducing drug U46619 was reduced. TMEM16A also was required for peripheral blood vessel contractility, as the response to U46619 was attenuated in isolated perfused hind limbs from mutant mice. Out data suggest that TMEM16A plays a general role in arteriolar and capillary blood flow and is a promising target for the treatment of hypertension.

AB - High blood pressure is the leading risk factor for death worldwide. One of the hallmarks is a rise of peripheral vascular resistance, which largely depends on arteriole tone. Ca2+-activated chloride currents (CaCCs) in vascular smooth muscle cells (VSMCs) are candidates for increasing vascular contractility. We analyzed the vascular tree and identified substantial CaCCs in VSMCs of the aorta and carotid arteries. CaCCs were small or absent in VSMCs of medium-sized vessels such as mesenteric arteries and larger retinal arterioles. In small vessels of the retina, brain, and skeletal muscle, where contractile intermediate cells or pericytes gradually replace VSMCs, CaCCs were particularly large. Targeted disruption of the calcium-activated chloride channel TMEM16A, also known as ANO1, in VSMCs, intermediate cells, and pericytes eliminated CaCCs in all vessels studied. Mice lacking vascular TMEM16A had lower systemic blood pressure and a decreased hypertensive response following vasoconstrictor treatment. There was no difference in contractility of medium-sized mesenteric arteries; however, responsiveness of the aorta and small retinal arterioles to the vasoconstriction-inducing drug U46619 was reduced. TMEM16A also was required for peripheral blood vessel contractility, as the response to U46619 was attenuated in isolated perfused hind limbs from mutant mice. Out data suggest that TMEM16A plays a general role in arteriolar and capillary blood flow and is a promising target for the treatment of hypertension.

KW - 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid

KW - Animals

KW - Arterioles

KW - Blood Pressure

KW - Brain

KW - Chloride Channels

KW - Cloning, Molecular

KW - DNA, Complementary

KW - Electrophysiology

KW - Estrogen Antagonists

KW - HEK293 Cells

KW - Humans

KW - Hypertension

KW - Membrane Potentials

KW - Mesenteric Arteries

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Muscle, Smooth, Vascular

KW - Neoplasm Proteins

KW - Pericytes

KW - Retina

KW - Tamoxifen

KW - Time Factors

KW - Vascular Resistance

KW - Vasoconstrictor Agents

U2 - 10.1172/JCI70025

DO - 10.1172/JCI70025

M3 - SCORING: Journal article

C2 - 24401273

VL - 124

SP - 675

EP - 686

JO - J CLIN INVEST

JF - J CLIN INVEST

SN - 0021-9738

IS - 2

ER -