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January 1, 2004AJP Heart and Circulatory Physiology

Inhibition of endothelium-dependent vasorelaxation by extracellular K+: a novel controlling signal for vascular contractility

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Population

Mouse aorta, mouse aorta endothelial cells (MAEC), and human umbilical vein endothelial cells (HUVEC)

Comparison

Increase in extracellular K+ concentration from… vs Baseline extracellular K+ concentration (6 mM)

Design

Preclinical

Authors

GSGeun Hee SeolKorea UniversitySASeung Cheol AhnDankook UniversityJKJi Aee KimEwha Womans University

Discussion

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Overview

Physiological [K+]o may suppress endothelial relaxation in vessels; leaves open relevance to human vascular tone or disease.

Structured PICO

P
Population
Mouse aorta, mouse aorta endothelial cells (MAEC), and human umbilical vein endothelial cells (HUVEC)
I
Intervention
Increase in extracellular K+ concentration ([K+]o) from 6 to 12 mM
C
Comparator
Baseline extracellular K+ concentration (6 mM)
O
Outcome
Endothelium-dependent relaxation (EDR) and intracellular Ca2+ concentration ([Ca2+]i)surrogate

Extracellular potassium in the physiological range acts as a controlling signal for vascular contractility by inhibiting endothelium-dependent vasorelaxation.

Cite This Study

Seol et al. (2004) studied this question.

synapsesocial.com/papers/6a2304ebc650520b07cb27ddhttps://doi.org/10.1152/ajpheart.00503.2003
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  5. 5Depolarization-mediated inhibition of Ca2+entry in endothelial cells1999 · 28 citations