Department of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Rende, Italy.
Maternal and Fetal Health Research Centre, Division of Developmental Biology and Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WL, UK.
Biomolecules. 2021 Jan 21;11(2):137. doi: 10.3390/biom11020137.
Recent evidence suggests that the reason Extra Virgin Olive Oil (EVOO) lowers blood pressure and reduces the risk of developing hypertension is partly due to minor components of EVOO, such as phenols. However, little is still known about the mechanism(s) through which EVOO phenols mediate anti-hypertensive effects. The aim of the present study was to investigate the mechanisms of action of EVOO phenols on mesenteric resistance arteries. A pressure myograph was used to test the effect of EVOO phenols on isolated mesenteric arteries in the presence of specific inhibitors of: 1) BKca channels (Paxillin, 10 M); 2) L-type calcium channels (Verapamil, 10 M); 3) Ryanodine receptor, RyR (Ryanodine, 10 M); 4) inositol 1,4,5-triphosphate receptor, IP3R, (2-Aminoethyl diphenylborinate, 2-APB, 3 × 10 M); 5) phospholipase C, PLC, (U73122, 10 M), and 6) GPCR-G signaling, (Pertussis Toxin, 10 M). EVOO phenols induced vasodilation of mesenteric arteries in a dose-dependent manner, and this effect was reduced by pre-incubation with Paxillin, Verapamil, Ryanodine, 2-APB, U73122, and Pertussis Toxin. Our data suggest that EVOO phenol-mediated vasodilation requires activation of BKca channels potentially through a local increase of subcellular calcium microdomains, a pivotal mechanism on the base of artery vasodilation. These findings provide novel mechanistic insights for understanding the vasodilatory properties of EVOO phenols on resistance arteries.
最近的证据表明，特级初榨橄榄油（EVOO）降低血压和降低高血压风险的部分原因是由于 EVOO 的一些次要成分，如酚类。然而，对于 EVOO 酚类通过何种机制来介导抗高血压作用，人们知之甚少。本研究旨在探讨 EVOO 酚类对肠系膜阻力动脉作用的机制。使用压力肌描记法在存在特定抑制剂的情况下测试 EVOO 酚类对分离的肠系膜动脉的作用：1）BKca 通道（Paxillin，10 M）；2）L 型钙通道（维拉帕米，10 M）；3）ryanodine 受体，RyR（Ryanodine，10 M）；4）肌醇 1,4,5-三磷酸受体，IP3R（2-氨基乙基二苯基硼酸盐，2-APB，3×10 M）；5）磷脂酶 C，PLC（U73122，10 M）和 6）GPCR-G 信号转导（百日咳毒素，10 M）。EVOO 酚类以剂量依赖的方式诱导肠系膜动脉扩张，这种作用可通过 Paxillin、维拉帕米、Ryanodine、2-APB、U73122 和百日咳毒素的预孵育而降低。我们的数据表明，EVOO 酚介导的血管舒张需要 BKca 通道的激活，这可能是通过细胞内钙微区的局部增加来实现的，这是动脉舒张的关键机制。这些发现为理解 EVOO 酚类对阻力动脉的血管舒张特性提供了新的机制见解。
