Fructose perfusion in rat mesenteric arteries impairs endothelium-dependent vasodilation

Joyce M. Richey, Xiaochen Si, Jeffrey B. Halter, R Clinton Webb

Research output: Contribution to journalArticle

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Abstract

We demonstrated that the fructose-induced hypertensive rat, representative of the principal metabolic abnormalities found in a majority of hypertensive patients, i.e. hypertriglyceridemia, hyperinsulinemia and insulin resistance (Syndrome X), is associated with an impaired response to endothelium-dependent vasodilators and that fructose may directly contribute to this impairment. Twelve male Wistar rats were divided into two groups, one given 10% fructose (n=6); the other no fructose (n=6) for 40 days in the drinking water. Systolic blood pressure was measured via the tail cuff method. Perfusion pressure responses to acetylcholine, were measured in the isolated perfused mesenteric vascular bed. Constrictor or dilator responses were measured as increases or decreases, respectively, of the perfusion pressure at a constant flow (4 ml/min). Fructose-fed rats had significantly higher blood pressure, insulin and triglyceride levels than control animals. In phenylephrine constricted beds, the endothelium-dependent dilatation to acetylcholine (0.001 to 1 μmol) was attenuated in the fructose-fed group compared to control animals. Whether this abnormality results from the syndromes (hyperinsulinemia, hypertension and hypertriglyceridemia) associated with the fructose-fed animal model is unknown. We therefore hypothesized that fructose can impair the endothelium-dependent vasodilator response. This was evaluated by perfusing mesenteric arteries from normal rats with control mannitol (40 mM) or fructose (40 mM). Endothelium-dependent dilation to acetylcholine was impaired in fructose-perfused mesenteric arteries. Indomethacin restored the vasodilator response to acetylcholine, suggesting that a cyclooxygenase derivative mediates the impaired response. Thus, we conclude that fructose can contribute to the impaired endothelium-dependent response in the fructose-induced hypertensive rat model.

Original languageEnglish (US)
JournalLife sciences
Volume62
Issue number4
StatePublished - Dec 19 1997

Fingerprint

Mesenteric Arteries
Fructose
Vasodilation
Endothelium
Rats
Perfusion
Acetylcholine
Endothelium-Dependent Relaxing Factors
Animals
Hypertriglyceridemia
Blood pressure
Hyperinsulinism
Dilatation
Metabolic Syndrome X
Insulin
Blood Pressure
Hypertension
Pressure
Level control
Mannitol

Keywords

  • Cyclooxygenase products
  • Endothelium-dependent relaxation
  • Fructose
  • Mesentery

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Fructose perfusion in rat mesenteric arteries impairs endothelium-dependent vasodilation. / Richey, Joyce M.; Si, Xiaochen; Halter, Jeffrey B.; Webb, R Clinton.

In: Life sciences, Vol. 62, No. 4, 19.12.1997.

Research output: Contribution to journalArticle

Richey, Joyce M. ; Si, Xiaochen ; Halter, Jeffrey B. ; Webb, R Clinton. / Fructose perfusion in rat mesenteric arteries impairs endothelium-dependent vasodilation. In: Life sciences. 1997 ; Vol. 62, No. 4.
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