Signaling of angiotensin II-induced vascular protein synthesis in conduit and resistance arteries in vivo

Daigle, C., Martens, F.M.A.C., Girardot, D., Dao, H., Touyz, R.M. and Moreau, P. (2004) Signaling of angiotensin II-induced vascular protein synthesis in conduit and resistance arteries in vivo. BMC Cardiovascular Disorders, 4(6), (doi: 10.1186/1471-2261-4-6)

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Abstract

<b>Background</b> From in vitro studies, it has become clear that several signaling cascades are involved in angiotensin II-induced cellular hypertrophy. The aim of the present study was to determine some of the signaling pathways mediating angiotensin II (Ang II)-induced protein synthesis in vivo in large and small arteries.<p></p> <b>Methods</b> Newly synthesized proteins were labeled during 4 hours with tritiated leucine in conscious control animals, or animals infused for 24 hours with angiotensin II (400 ng/kg/min). Hemodynamic parameters were measure simultaneously. Pharmacological agents affecting signaling cascades were injected 5 hours before the end of Ang II infusion.<p></p> <b>Results</b> Angiotensin II nearly doubled the protein synthesis rate in the aorta and small mesenteric arteries, without affecting arterial pressure. The AT1 receptor antagonist Irbesartan antagonized the actions of Ang II. The Ang II-induced protein synthesis was associated with increased extracellular signal-regulated kinases (ERK)1/2 phosphorylation in aortic, but not in mesenteric vessels. Systemic administration of PD98059, an inhibitor of the ERK-1/2 pathway, produced a significant reduction of protein synthesis rate in the aorta, and only a modest decrease in mesenteric arteries. Rapamycin, which influences protein synthesis by alternative signaling, had a significant effect in both vessel types. Rapamycin and PD98059 did not alter basal protein synthesis and had minimal effects on arterial pressure.<p></p> <b>Conclusion</b> ERK1/2 and rapamycin-sensitive pathways are involved in pressure-independent angiotensin II-induced vascular protein synthesis in vivo. However, their relative contribution may vary depending on the nature of the artery under investigation.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Touyz, Professor Rhian
Authors: Daigle, C., Martens, F.M.A.C., Girardot, D., Dao, H., Touyz, R.M., and Moreau, P.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:BMC Cardiovascular Disorders
ISSN:1471-2261
ISSN (Online):1471-2261
Published Online:10 May 2004
Copyright Holders:Copyright © 2004 The Author
First Published:First published in BMC Cardiovascular Disorders 4:6
Publisher Policy:Reproduced in accordance with the copyright policy of the publisher

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