Fructose Intake Impairs the Synergistic Vasomotor Manifestation of Nitric Oxide and Hydrogen Sulfide in Rat Aorta

• Published in: International journal of molecular sciences 2021-04, Vol.22 (9), p.4749
• Main Authors: Berenyiova, Andrea, Golas, Samuel, Drobna, Magdalena, Cebova, Martina, Cacanyiova, Sona
• Format: Article
• Language: English
• Subjects: Adrenergic receptors; Alanine; Alanine transaminase; Animals; Aorta; Aorta, Thoracic - drug effects; Aorta, Thoracic - physiology; Blood glucose; Blood pressure; Blood Pressure - drug effects; Cholesterol; Contraction; Coronary vessels; Dietary Sugars - administration & dosage; Dietary Sugars - metabolism; Endothelium; Endothelium-Dependent Relaxing Factors - metabolism; Endothelium-Dependent Relaxing Factors - pharmacology; Enzymes; Food; Fructose; Fructose - administration & dosage; Fructose - metabolism; Gasotransmitters - metabolism; Gasotransmitters - pharmacology; Glucose; Hydrogen sulfide; Hydrogen Sulfide - metabolism; Hydrogen Sulfide - pharmacology; Male; Metabolic disorders; Metabolic syndrome; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide - pharmacology; Nitric-oxide synthase; Noradrenaline; Norepinephrine; Plasma levels; Rats; Rats, Inbred WKY; Receptors (physiology); Sensitivity; Signal Transduction - drug effects; thoracic aorta; Thorax; Transaminase; Tumor necrosis factor-TNF; Vasoactive agents; Vasodilation; Vasodilation - drug effects; Ventricle; Wistar Kyoto rats
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22094749

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 H S. 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 H S 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-H S interaction and its manifestation in vasoactive responses.