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Endothelial dependent dilation by estrogen through the AKTPKB pathway

Acute administration of estrogen results in the vasodilatation and in the release of nitric oxide (NO) that occurs through activation of the serine-threonine kinase Akt/protein-kinase-B (PKB), which is known to increase the eNOS activity. 10-8 M of 17-beta-estradiol resulted in a left shift of the vasodilatory response to Ach in preconstricted aortic rings from oophorectomized rats (EC50 = 0.7 x 10-8 M with 17-beta-estradiol and 0.15 x 10-7 M of Ach without 17-beta-estradiol, P < 0.05). The effect was blocked by pre-treatment with Wortmannin, a PI(3)K inhibitor. AKT/PKB was phosphorylated in endothelial cells (EC) as early as 1-minute after estradiol-stimulation. Phosphorylation of eNOS and NO release in EC treated with 17-beta-estradiol were also increased. We conclude that the AKT/PKB pathway is involved in the acute release of NO by estrogen.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.33757
Date January 2001
CreatorsFlórián, Mária, 1953-
ContributorsMagder, Sheldon (advisor)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageMaster of Science (Department of Physiology.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001862509, proquestno: MQ78874, Theses scanned by UMI/ProQuest.

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