Fructose Intake Impairs the Synergistic Vasomotor Manifestation of Nitric Oxide and Hydrogen Sulfide in Rat Aorta
| Autor: | M Drobna, Sona Cacanyiova, Samuel Golas, Martina Cebova, Andrea Berenyiova |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
0301 basic medicine Dietary Sugars hydrogen sulfide Adrenergic Aorta Thoracic Blood Pressure Rats Inbred WKY 030226 pharmacology & pharmacy fructose chemistry.chemical_compound 0302 clinical medicine thoracic aorta Enos Thoracic aorta Biology (General) Spectroscopy biology Gasotransmitters General Medicine Computer Science Applications Vasodilation Chemistry Signal Transduction medicine.medical_specialty Adrenergic receptor QH301-705.5 Article Catalysis Nitric oxide Inorganic Chemistry 03 medical and health sciences nitric oxide medicine.artery Internal medicine medicine Animals Physical and Theoretical Chemistry Molecular Biology QD1-999 Endothelium-Dependent Relaxing Factors Organic Chemistry Fructose biology.organism_classification 030104 developmental biology Endocrinology chemistry Alanine transaminase biology.protein Wistar Kyoto rats Lipoprotein |
| Zdroj: | International Journal of Molecular Sciences, Vol 22, Iss 4749, p 4749 (2021) International Journal of Molecular Sciences Volume 22 Issue 9 |
| ISSN: | 1661-6596 1422-0067 |
| Popis: | In this study, we evaluated the effect of eight weeks of administration of 10% fructose solution to adult Wistar Kyoto (WKY) rats on systolic blood pressure (SBP), plasma and biometric parameters, vasoactive properties of the thoracic aorta (TA), NO synthase (NOS) activity, and the expression of enzymes producing NO and H2S. Eight weeks of fructose administration did not affect SBP, glycaemia, or the plasma levels of total cholesterol or low-density and high-density lipoprotein however, it significantly increased the plasma levels of γ-glutamyl transferase and alanine transaminase. Chronic fructose intake deteriorated endothelium-dependent vasorelaxation (EDVR) and increased the sensitivity of adrenergic receptors to noradrenaline. Acute NOS inhibition evoked a reduction in EDVR that was similar between groups however, it increased adrenergic contraction more in fructose-fed rats. CSE inhibition decreased EDVR in WKY but not in fructose-fed rats. The application of a H2S scavenger evoked a reduction in the EDVR in WKY rats and normalized the sensitivity of adrenergic receptors in rats treated with fructose. Fructose intake did not change NOS activity but reduced the expression of eNOS and CBS in the TA and CSE and CBS in the left ventricle. Based on our results, we could assume that the impaired vascular function induced by increased fructose intake was probably not directly associated with a decreased production of NO, but rather with impairment of the NO–H2S interaction and its manifestation in vasoactive responses. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|