Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor.

Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Research Abstract Details 

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Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Abstract Text:

Hiroyuki Suzuki,Kunie Eguchi,Haruhiko Ohtsu,Sadaharu Higuchi,Sudhir Dhobale,Gerald D Frank,Evangeline D Motley,Satoru Eguchi,

Enhanced angiotensin II (AngII) action has been implicated in endothelial dysfunction that is characterized as decreased nitric oxide availability. Although endothelial cells have been reported to express AngII type 1 (AT1) receptors, the exact role of AT1 in regulating endothelial NO synthase (eNOS) activity remains unclear. We investigated the possible regulation of eNOS through AT1 in bovine aortic endothelial cells (BAECs) and its functional significance in rat aortic vascular smooth muscle cells (VSMCs). In BAECs infected with adenovirus encoding AT1 and in VSMCs infected with adenovirus encoding eNOS, AngII rapidly stimulated phosphorylation of eNOS at Ser1179. This was accompanied with increased cGMP production. These effects were blocked by an AT1 antagonist. The cGMP production was abolished by a NOS inhibitor as well. To explore the importance of eNOS phosphorylation, VSMCs were also infected with adenovirus encoding S1179A-eNOS. AngII did not stimulate cGMP production in VSMCs expressing S1179A. However, S1179A was able to enhance basal NO production as confirmed with cGMP production and enhanced vasodilator-stimulated phosphoprotein phosphorylation. Interestingly, S1179A prevented the hypertrophic response similar to wild type in VSMCs. From these data, we conclude that the AngII/AT1 system positively couples to eNOS via Ser1179 phosphorylation in ECs and VSMCs if eNOS and AT1 coexist. However, basal level NO production may be sufficient for prevention of AngII-induced hypertrophy by eNOS expression. These data demonstrate a novel molecular mechanism of eNOS regulation and function and thus provide useful information for eNOS gene therapy under endothelial dysfunction.

Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Publishing Authors By Initials

H Suzuki,K Eguchi,H Ohtsu,S Higuchi,S Dhobale,GD Frank,ED Motley,S Eguchi,

For similar investigative techniques: genetic techniques: gene transfer techniques: transfection research abstracts see: investigative techniques: genetic techniques: gene transfer techniques: transfection research

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Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Endocrinology

VOLUME: 147

Page Numbers: 5914-20

Journal Abbreviation: Endocrinology

ISSN: 0013-7227

DAY: 15

MONTH: 09

YEAR: 2006

Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375040

Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Keywords Mesh Terms:

KEYWORDS: Transfection

MESH TERMS: physiology

Chemical & Substance for Abstract: Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor. Information

Substance Name: Nitric Oxide Synthase Type III

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Activation of endothelial nitric oxide synthase by the angiotensin II type 1 receptor.

AFFILIATION: Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, Pennsylvania 19140, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL076770

ACRONYM: HL

MEDLINETA: Endocrinology

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