Skip Navigation

Cardiovascular Research 1998 39(3):657-664; doi:10.1016/S0008-6363(98)00151-5
© 1998 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Iglarz, M.
Right arrow Articles by Henrion, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Iglarz, M.
Right arrow Articles by Henrion, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1998, European Society of Cardiology

Chronic blockade of endothelin ETA receptors improves flow dependent dilation in resistance arteries of hypertensive rats

Marc Iglarz, Khalid Matrougui, Bernard I. Lévy and Daniel Henrion*

Institut National de la Santé et de la Recherche Médicale (INSERM) U 141, IFR 6 (Circulation-Lariboisière), Université Paris VII, Hôpital Lariboisière, 41, Bd de la Chapelle, 75475 Paris, Cedex 10, France

* Corresponding author. Tel.: +33-1-4463-1864; Fax: +33-1-4281-3128; E-mail: daniel.henrion@inserm.lrb.ap-hop-paris.fr

Objective: Flow (shear stress)-induced dilation (FD) is attenuated in hypertension. Flow triggers the release by endothelial cells of dilators, such as NO or cyclo-oxygenase (COX) derivatives and constrictor factors such as endothelin-1 (ET-1) which might be involved in several cardiovascular diseases. We hypothesized that ET-1 might play a functional role in FD and participate in the endothelial dysfunction in hypertension. Methods: We investigated the effect of a chronic treatment with the ETA receptor blocker LU135252 (50 mg/kg/day) for 2 weeks on the dilator response to flow in normotensive (Wistar–Kyoto; WKY) or hypertensive (SHR, n=7 or 8 per group) rats. Results: Systolic arterial pressure was not significantly affected by chronic ETA receptor blockade in both strains. In mesenteric resistance arteries (diameter: approximately 100 µm), isolated in vitro, FD was lower and myogenic tone higher in SHR than in WKY rats. Chronic ETA receptor blockade increased FD by 73% (7.5±1.5 to 13.0±2.7 µm dilation with a flow-rate of 150 µl/min) in SHR (no effect in WKY). The participation of NO to FD was increased in SHR and the participation of dilator COX product(s) (blocked by indomethacin 10 µmol/l) to FD was significantly increased in SHR and in WKY. In control rats FD was improved by acute ETA receptor blockade in WKY rats (18.5±2.0 to 23.2±1.8 µm dilation to flow-rate of 150 µl/min) and significantly more in SHR (6.0±1.8 to 15.1±1.6 µm). Acetylcholine-induced dilation was also improved by chronic ETA receptor blockade (no effect of an acute blockade). Myogenic and phenylephrine-induced tone were not affected by chronic or acute ETA receptor blockade. The improvement of endothelium-dependent dilation was not related to a change in blood pressure Conclusion: Chronic ETA receptor blockade increased flow-induced dilation in SHR possibly by suppressing flow-induced ETA stimulation and by improving the release of dilator products by the endothelium.

KEYWORDS Flow; Shear stress; Dilation; Myogenic tone; Resistance arteries; Indomethacin; L-NAME; Endothelin-1; Hypertension; WKY rats; SHR rats


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
S. Mateev, A. H. Sillau, R. Mouser, R. E. McCullough, M. M. White, D. A. Young, and L. G. Moore
Chronic hypoxia opposes pregnancy-induced increase in uterine artery vasodilator response to flow
Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H820 - H829.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
L. B. Tanko and K. Matrougui
Can We Apply Results From Large to Small Arteries?
Circ. Res., March 22, 2002; 90 (5): e68 - e68.
[Full Text] [PDF]

Home page
 HypertensionHome page
M. Iglarz, J. Benessiano, I. Philip, S. Vuillaumier-Barrot, S. Lasocki, U. Hvass, G. Durand, J.-M. Desmonts, B. I. Levy, and D. Henrion
Preproendothelin-1 Gene Polymorphism Is Related to a Change in Vascular Reactivity in the Human Mammary Artery In Vitro
Hypertension, February 1, 2002; 39(2): 209 - 213.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
R. Berger, B. Stanek, M. Hulsmann, B. Frey, S. Heher, R. Pacher, and T. Neunteufl
Effects of Endothelin A Receptor Blockade on Endothelial Function in Patients With Chronic Heart Failure
Circulation, February 20, 2001; 103(7): 981 - 986.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
A. Huang, D. Sun, and A. Koller
Shear Stress-Induced Release of Prostaglandin H2 in Arterioles of Hypertensive Rats
Hypertension, April 1, 2000; 35(4): 925 - 930.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
R. Parent and M. Lavallee
Endothelin-dependent effects limit flow-induced dilation of conductance coronary vessels after blockade of nitric oxide formation in conscious dogs
Cardiovasc Res, January 14, 2000; 45(2): 470 - 477.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.