Vasorelaxant effect of monoterpene carvacrol on isolated human umbilical artery
Author(s) -
Đorđe Đukanović,
Milica Gajić Bojić,
Sonja Marinković,
Saša M. Trailović,
Miloš P. Stojiljković,
Ranko Škrbić
Publication year - 2022
Publication title -
canadian journal of physiology and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.559
H-Index - 84
eISSN - 1205-7541
pISSN - 0008-4212
DOI - 10.1139/cjpp-2021-0736
Subject(s) - vasodilation , chemistry , contraction (grammar) , antispasmodic , antagonist , vascular smooth muscle , bicarbonate , mechanism of action , pharmacology , nifedipine , endocrinology , medicine , anesthesia , biochemistry , smooth muscle , calcium , receptor , in vitro
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 EC 50 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 BaCl 2 -induced contraction in Ca 2+ -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 TRPV 3 channel, was able to decrease the efficacy of CRV ( p < 0.001). The blocking of L-type Ca 2+ channels on smooth muscle cells is the most probable mechanism of CRV-induced vasorelaxation. However, the role of TRPV 3 channels in CRV-induced vasodilation of HUA cannot be excluded either.
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