Diminished NO release in chronic hypoxic human endothelial cells.

Diminished NO release in chronic hypoxic human endothelial cells. Research Abstract Details 

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Diminished NO release in chronic hypoxic human endothelial cells. Abstract Text:

Louise Ostergaard,Edgaras Stankevicius,Malene R Andersen,Yvonne Eskildsen-Helmond,Thomas Ledet,Michael J Mulvany,Ulf Simonsen,Louise Ostergaard,Edgaras Stankevicius,Malene R Andersen,Yvonne Eskildsen-Helmond,Thomas Ledet,Michael J Mulvany,Ulf Simonsen,

The present study addressed whether chronic hypoxia is associated with reduced nitric oxide (NO) release due to decreased activation of endothelial NO synthase (eNOS). Primary cultures of endothelial cells from human umbilical veins (HUVECs) were used and exposed to different oxygen levels for 24 h, after which NO release, intracellular calcium, and eNOS activity and phosphorylation were measured after 24 h. Direct measurements using a NO microsensor showed that in contrast to 1-h exposure to 5% and 1% oxygen (acute hypoxia), histamine-evoked (10 microM) NO release from endothelial cells exposed to 5% and 1% oxygen for 24 h (chronic hypoxia) was reduced by, respectively, 58% and 40%. Furthermore, chronic hypoxia also lowered the amount and activity of eNOS enzyme. The decrease in activity could be accounted for by reduced intracellular calcium and altered eNOS phosphorylation. eNOS Ser(1177) and eNOS Thr(495) phosphorylations were reduced and increased, respectively, consistent with lowered enzyme activity. Akt kinase, which can phosphorylate eNOS Ser(1177), was also decreased by hypoxia, regarding both total protein content and the phosphorylated (active) form. Moreover, the protein content of beta- actin, which is known to influence the activity of eNOS, was almost halved by hypoxia, further supporting the fall in eNOS activity. In conclusion, chronic hypoxia in HUVECs reduces histamine-induced NO release as well as eNOS expression and activity. The decreased activity is most likely due to changed eNOS phosphorylation, which is supported by decreases in Akt expression and phosphorylation. By reducing NO, chronic hypoxia may accentuate endothelial dysfunction in cardiovascular disease.

Diminished NO release in chronic hypoxic human endothelial cells. Publishing Authors By Initials

L Ostergaard,E Stankevicius,MR Andersen,Y Eskildsen-Helmond,T Ledet,MJ Mulvany,U Simonsen,L Ostergaard,E Stankevicius,MR Andersen,Y Eskildsen-Helmond,T Ledet,MJ Mulvany,U Simonsen,

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Diminished NO release in chronic hypoxic human endothelial cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Heart and circulat

VOLUME: 293

Page Numbers: H2894-903

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 24

MONTH: 08

YEAR: 2007

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LANGUAGE: eng

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Grant and Affiliation Information for Diminished NO release in chronic hypoxic human endothelial cells.

AFFILIATION: Department of Pharmacology, University of Aarhus, Aarhus, Denmark.

Country: United States

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MEDLINETA: Am J Physiol Heart Circ Physio

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