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Peredo HA, Mayer M, Faya IR, et al. Dehydroepiandrosterone (DHEA) prevents the prostanoid imbalance in mesenteric bed of fructose-induced hypertensive rats. Eur J Nutr. 2008;47(7):349-56doi: 10.1007/s00394-008-0734-7.
Peredo, H. A., Mayer, M., Faya, I. R., Puyó, A. M., & Carranza, A. (2008). Dehydroepiandrosterone (DHEA) prevents the prostanoid imbalance in mesenteric bed of fructose-induced hypertensive rats. European journal of nutrition, 47(7), 349-56. https://doi.org/10.1007/s00394-008-0734-7
Peredo, Horacio A, et al. "Dehydroepiandrosterone (DHEA) prevents the prostanoid imbalance in mesenteric bed of fructose-induced hypertensive rats." European journal of nutrition vol. 47,7 (2008): 349-56. doi: https://doi.org/10.1007/s00394-008-0734-7
Peredo HA, Mayer M, Faya IR, Puyó AM, Carranza A. Dehydroepiandrosterone (DHEA) prevents the prostanoid imbalance in mesenteric bed of fructose-induced hypertensive rats. Eur J Nutr. 2008 Oct;47(7):349-56. doi: 10.1007/s00394-008-0734-7. Epub 2008 Aug 25. PMID: 18726563.
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Eur J Nutr. 2008 Oct;47(7):349-56. doi: 10.1007/s00394-008-0734-7. Epub 2008 Aug 25.

Dehydroepiandrosterone (DHEA) prevents the prostanoid imbalance in mesenteric bed of fructose-induced hypertensive rats.

European journal of nutrition

Horacio A Peredo, Marcos Mayer, Ileana R Faya, Ana M Puyó, Andrea Carranza

Affiliations

  1. Dept. of Pharmatechnology I, Faculty of Pharmacy and Biochemistry, INFIBIOC, University of Buenos Aires, Buenos Aires, Argentina.

PMID: 18726563 DOI: 10.1007/s00394-008-0734-7

Abstract

BACKGROUND: In previous studies we reported an altered prostanoid (PR) release-pattern in mesenteric vessels in fructose (F)-overloaded rats, an experimental model of insulin resistance and hypertension. Dehydroepiandrosterone (DHEA) and its precursor Dehydroepiandrosterone sulfate (DHEA-S) are the most abundant circulating steroid hormones produced by the adrenal and recent studies in both cells and animals suggest that DHEA may have acute non-genomic actions that mimic both metabolic and vascular actions of insulin.

AIM OF THE STUDY: This study was to analyze in F-overloaded rats, the effects of DHEA treatment on arterial blood pressure and the PR production in mesenteric vessels and aorta.

METHODS: Male 6 week-old Sprague-Dawley rats were randomly divided in four groups: a control group (C), a DHEA (30 mg/kg/sc/48 h)-treated group (D), a fructose (10% w/v in drinking water)-fed group (F), and both treatments simultaneously group (FD). The systolic blood pressure (SBP) was measured by tail cuff method and glycemia and triglyderidemia were measured by enzymatic assays. The mesenteric beds of all groups were dissected, and incubated in Krebs solution. The PR released were measured by HPLC.

RESULTS: F overload increased SBP and triglyceridemia and decreased the mesenteric vasodilatory PR release. DHEA treatment prevented the increment in SBP and triglyceridemia and decreased vasoconstrictor PR in F-treated rats.

CONCLUSION: DHEA normalize the PGI(2)/TX ratio, diminished in F-overloaded rats, through the decrease in thromboxane (TX) production and this could be one of the mechanisms by which DHEA prevented the slight hypertension in F-animals.

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