RESEARCH ARTICLE


Effects of Eprosartan on Serum Metabolic Parameters in Patients with Essential Hypertension



Evangelos C. Rizos1, Athanasia Spyrou1, Evangelos N. Liberopoulos1, Eleni C. Papavasiliou2, Vasilis Saougos1, Alexandros D. Tselepis2, Moses Elisaf1, *
1 Department of Internal Medicine, Medical School, University of Ioannina, 45110 Ioannina, Greece
2 Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, 45110 Ioannina, Greece

Article Information


Identifiers and Pagination:

Year: 2007
Volume: 1
First Page: 22
Last Page: 26
Publisher ID: TOCMJ-1-22
DOI: 10.2174/1874192400701010022

Article History:

Received Date: 26/9/2007
Revision Received Date: 1/10/2007
Acceptance Date: 2/10/2007
Electronic publication date: 14/11/2007
Collection year: 2007

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Creative Commons License
2007 Bentham Science Publishers Ltd.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

* Department of Internal Medicine, Medical School, University of Ioannina, 451 10 Ioannina, Greece; Tel: +302651097509; Fax: +302651097016; E-mailegepi@cc.uoi.gr


Abstract

The effect of the anti-hypertensive drug eprosartan on metabolic parameters is currently not extensively documented. We evaluated the effect of eprosartan on parameters involved in atherogenesis, oxidative stress and clotting activity. This open-label unblinded intervention study included 40 adult patients with essential hypertension taking eprosartan. Eprosartan significantly reduced by 8% (p<0.001) the systolic and by 13% (p<.001) the diastolic blood pressure, and in-creased by 24% the time needed to produce oxidative by-products (p=0.001), a marker of oxidative stress. In contrast, ep-rosartan did not alter 8-isoprostane (8-epiPGF2a) levels, another marker of oxidative stress. Additionally, eprosartan re-duced by 14% aspartate aminotransferase and by 21% then alanine aminotransferase activity, while it had a neutral effect on the lipid profile and apolipoprotein levels and did not influence glucose homeostasis, creatinine and uric acid levels. Eprosartan did not affect the clotting/fibrinolytic status (estimated by plasminogen activator inhibitor 1, tissue plasmino-gen activator and a2 antiplasmin levels), or the enzymatic activity of the lipoprotein associated phospholipase A2 (Lp-PLA2) and paraoxonase 1 (PON1). In conclusion, eprosartan should be mainly considered as an anti-hypertensive agent with neutral effects on most of the metabolic parameters in hypertensive patients.

Keywords: Eprosartan, hypertension, isoprostane, cholesterol, lipoprotein associated phospholipase A2, glucose.