Glycerol Increases Fructose-Induced Hypertension in Rats

pp 87-92

Authors

  • Pablo F. Damiano Depto. de Fisiología, Facultad de Medicina, Universidad de Buenos Aires
  • María I. Roson Depto. de Fisiología, Facultad de Medicina, Universidad de Buenos Aires
  • Eduardo Dascal Centro de Investigaciones Endocrinológicas, Hospital de Pediatría R. Gutiérrez.
  • Luis Cuniberti Centro de Investigaciones Endocrinológicas, Hospital de Pediatría R. Gutiérrez.
  • Liliana E. Albornoz Depto. de Fisiología, Facultad de Medicina, Universidad de Buenos Aires
  • Ana M. Puyo Universidad Favaloro, Buenos Aires, Argentina.
  • Ignacio J. De la Riva Depto. de Fisiología, Facultad de Medicina, Universidad de Buenos Aires

DOI:

https://doi.org/10.7775/rac.v68i1.3098

Keywords:

Arterial hypertension, Hyperinsulinemia, Protein kinase-C (PKC), Vascular contractility

Abstract

A fructose-enriched diet is known to promote arterial hypertension in the rats. The aim of this study was to evaluate blood pressure changes induced by glycolipidic alterations related to hypertension. Four groups of rats were studied:1)controls (C),fed with a standard diet and tap water; 2) glycerol (G), maintained on a standard diet with the addition of 5% glycerol in tap water; 3)fructose (F), fed with 55% fructose in the diet; and 4) fructose + glycerol (FG), the same diet of F plus 5% glycerol in tap water. At the end of the second week the results wereas follows: blood pressure and insuline-mia increased in FG vs. C, G and F groups. Triglyceridemia increased in FG, F and G groups vs C one. Aorta rings showed a lower ED, to phorbol 12,13-dibutirate (PDBu) in FG vs. C group. There was a high positive correlation between ED., PDBu and BP (r = 0.69 r2=0.48).We conclude that glycerol administration to rats on a diet rich in fructose, potentiates the development of hypertension. Furthermore, correlations between ED50 to PIDBu-insulinemia, and between ED50 to PDBU-BP suggests a role forPKC in the mechanisms leading to the blood pressure elevations.

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Published

2026-03-11

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Section

ORIGINAL ARTICLES

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