Placenta · 2026
Eucalyptol (1,8-cineole) relaxes umbilical veins in normoglycemic parturients and parturients with gestational diabetes mellitus by modulating ion channels: An ex vivo study.
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de Sousa Machado Sara Tavares, Batista Paulo Ricardo, da Silva Franscisca Daliane Severino, Pereira-de-Morais Luís, Magalhães Laíza Maria Ulisses, Barbosa Roseli
Аннотация
INTRODUCTION: The monoterpenoid eucalyptol (EUC; 1,8-cineole) has a vasodilatory effect on rat arteries; however, its effects on the human fetoplacental vasculature had not yet been described. Thus, the objective of this study is to evaluate the endothelium-independent vasorelaxant effect of EUC on human umbilical veins from normoglycemic parturients (HUV-NG) and parturients with gestational diabetes mellitus (HUV-GDM).
METHOD: Denuded HUV rings were mounted in organ bath for isometric recordings under different experimental protocols in the presence of EUC (1-3000 μM).
RESULTS: EUC (1-3000 μM) inhibited vasoconstriction induced by KCl (60 mM) and 5-HT (10 μM), exhibiting greater potency in HUV-GDM. EUC (3000 μM) prevented vasoconstriction induced by CaCl2 or BaCl2 (0.1-30 mM) in HUV-NG. However, its efficacy in preventing vasoconstriction induced by high concentrations of BaCl2 was attenuated in HUV-GDM. The presence of potassium channel blockers (TEA, 4-AP, GLI, and BaCl2) reduced the vasorelaxant efficacy and potency of EUC, differentially in HUV-NG and HUV-GDM.
DISCUSSION: The results suggest that EUC acts by modulating ion channels to induce vasorelaxation in HUV, possibly through the inhibition of voltage-operated calcium channels and the activation of potassium channels in vascular smooth muscle. Furthermore, the pathophysiological changes induced by GDM in HUV appear to alter the pharmacodynamics of EUC; nevertheless, the vasorelaxant effect of EUC was more potent via electromechanical and pharmacomechanical pathways in HUV-GDM. Thus, the current study provides a basis for the development of new pharmacological vasodilator strategies.
METHOD: Denuded HUV rings were mounted in organ bath for isometric recordings under different experimental protocols in the presence of EUC (1-3000 μM).
RESULTS: EUC (1-3000 μM) inhibited vasoconstriction induced by KCl (60 mM) and 5-HT (10 μM), exhibiting greater potency in HUV-GDM. EUC (3000 μM) prevented vasoconstriction induced by CaCl2 or BaCl2 (0.1-30 mM) in HUV-NG. However, its efficacy in preventing vasoconstriction induced by high concentrations of BaCl2 was attenuated in HUV-GDM. The presence of potassium channel blockers (TEA, 4-AP, GLI, and BaCl2) reduced the vasorelaxant efficacy and potency of EUC, differentially in HUV-NG and HUV-GDM.
DISCUSSION: The results suggest that EUC acts by modulating ion channels to induce vasorelaxation in HUV, possibly through the inhibition of voltage-operated calcium channels and the activation of potassium channels in vascular smooth muscle. Furthermore, the pathophysiological changes induced by GDM in HUV appear to alter the pharmacodynamics of EUC; nevertheless, the vasorelaxant effect of EUC was more potent via electromechanical and pharmacomechanical pathways in HUV-GDM. Thus, the current study provides a basis for the development of new pharmacological vasodilator strategies.