Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain


THE PATHOPHYSIOLOGICAL ROLE OF ALDOSTERONE IN THE VASCULAR SYSTEM.
Abstract number: S43

Cachofeiro1 V, de las Heras1 N, Miana1 M, Martin-Fernandez1 B, Lahera1 V

1Departamento de Fisiologa, Facultad de Medicina, Universidad Complutense, Madrid

Aldosterone not only contributes to salt and water homeostasis, but also exerts direct cardiovascular effects. Many studies showed local extraadrenal production of aldosterone in brain, blood vessel, and the heart, which contribute in an important manner to the patological actions of this mineralocorticoid.

Objective: 

The aim of the present study was to evaluate the effect of the aldosterone receptor antagonist eplerenone in the vascular functional and structural alterations associated with hypertension.

Methods: 

Spontaneously hypertensive rats (SHR) were treated with either vehicle or eplerenone, a mineralocorticoid receptor antagonist, at two different doses 30 mg/kg/day and 100 mg/kg/day), for 10 weeks. Age-matched Wistar Kyoto rats (WKY) were used as a normotensive reference group.

Results: 

High blood-pressure levels were associated with endothelial dysfunction, oxidative stress, a decrease eNOS aorta gene expression and an increase in aortic IL1b, IL-6 and TNFa mRNA levels. SHR also showed an increase in aortic media/lumen ratio as compared with WKY. Both doses of eplerenone ameliorated endothelial function, decreased oxidative stress, normalized aortic media/lumen ratio, enhanced eNOS mRNA and decreased vascular cytokine gene expression to a similar extent. However, only the high dose of eplerenone was able to reduce blood pressure levels.

Conclusions: 

These data show that aldosterone through hemodynamic and non-hemodynamic mechanisms participates in hypertension-associated vascular damage in rats. This effect seems to involve stimulation of both inflammatory and fibrotic processes as well as oxidative stress that triggered endothelial dysfunction, an inflammatory process and vascular remodeling.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :S43

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE