Sulodexide Inhibits Arterial Contraction via the Endothelium-Dependent Nitric Oxide Pathway

Area of Science:

• Vascular biology
• Pharmacology
• Cardiovascular research

Background:

• Endothelial dysfunction contributes to arterial pathologies and impaired vasodilation.
• Sulodexide (SDX) is known for glycocalyx restoration, endothelial protection, and antithrombotic effects.
• Endothelial nitric oxide (NO) production is vital for vascular homeostasis.

Purpose of the Study:

• To investigate the effects of SDX on stimulated vascular tonus in human arteries.
• To assess the role of the endothelium and nitric oxide (NO) pathways in SDX's vasodilatory action.

Main Methods:

• Human internal mammary artery rings were used, divided into endothelium-intact and endothelium-denuded groups.
• Arterial contraction was measured before and after phenylephrine stimulation, with cumulative SDX doses applied.
• Nitric oxide synthase inhibition (L-NAME) was employed to evaluate the NO pathway's involvement.

Main Results:

• SDX induced concentration-dependent vasorelaxation in both endothelium-intact and denuded arterial rings.
• The vasorelaxant effect of SDX was significantly more pronounced in endothelium-intact rings at higher concentrations.
• SDX's inhibitory effect on contraction was similar in both groups after L-NAME pre-incubation, indicating NO pathway dependency.

Conclusions:

• SDX exerts a concentration-dependent inhibition of arterial contraction.
• An intact endothelium and NO-mediated pathways are crucial for SDX's vasodilatory effects.
• SDX shows potential therapeutic value for conditions involving endothelial dysfunction.