Vasorelaxant effect of monoterpene carvacrol on isolated human umbilical artery

Author:

Đukanović Đorđe1,Bojić Milica Gajić1,Marinković Sonja1,Trailović Saša2,Stojiljković Miloš P.13,Škrbić Ranko13

Affiliation:

1. Centre for Biomedical Research, Faculty of Medicine, University of Banja Luka, Banja Luka, The Republic of Srpska 78000, Bosnia and Herzegovina

2. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Belgrade, Belgrade 11 000, Serbia

3. Department of Pharmacology, Toxicology and Clinical Pharmacology, Faculty of Medicine, University of Banja Luka, Banja Luka, The Republic of Srpska, 78000, Bosnia and Herzegovina

Abstract

Carvacrol (CRV) is the main compound of essential oils extracted primarily from Thymus and Origanum species. Its various biological activities were confirmed: antioxidant, anti-inflammatory, antibacterial, antifungal, anti-tumour, antinematodal, and vasorelaxant action. Although vasodilation mediated by CRV was previously described, the exact mechanism of its action has not yet been established. Hence, the aim of this study was to investigate CRV vasoactivity on human umbilical arteries (HUA) and the different pathways involved in its mechanism of action using the tissue bath methodology. CRV caused a significant decrease in vascular tension of 5-HT-pre-contracted umbilical arteries, with EC50 of 442.13 ± 33.8 µmol/L (mean ± standard error of the mean—SEM). At 300 µmol/L, CRV shifted downward the 5-HT concentration–response curve with a statistical significance of p < 0.001 obtained for the four highest concentrations. At a concentration of 1 mmol/L, CRV completely abolished BaCl2-induced contraction in Ca2+-free Krebs–Ringer bicarbonate solution and the BAY K 8644-induced contraction in Krebs–Ringer bicarbonate solution ( p < 0.001). Isopentenyl pyrophosphate, the antagonist of TRPV3 channel, was able to decrease the efficacy of CRV ( p < 0.001). The blocking of L-type Ca2+ channels on smooth muscle cells is the most probable mechanism of CRV-induced vasorelaxation. However, the role of TRPV3 channels in CRV-induced vasodilation of HUA cannot be excluded either.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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