ArticleJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi2014
Inhibition of As(III) and Hg(II) caused aortic hypercontraction by eugenol, linalool and carvone.
Article in Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular Targets and Biological Activities of Carvone: An Evidence-Graded Review.Molecules (Basel, Switzerland) · 2026Review
- Monoterpenes in Vascular Function: A Review of Bioactivity and Mechanisms of Action.International journal of molecular sciences · 2025Review
- Aromatic Plant-Based Functional Foods: A Natural Approach to Manage Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2023Review
- Review
- Article
- Quercetin and resveratrol ameliorate nickel-mediated hypercontraction in isolated Wistar rat aorta.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Article
- The Role of Essential Oils and Their Main Compounds in the Management of Cardiovascular Disease Risk Factors.Molecules (Basel, Switzerland) · 2021Review
- Cardiovascular Activity of the Chemical Constituents of Essential Oils.Molecules (Basel, Switzerland) · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute and chronic exposure to arsenic and mercury is known to produce vasoconstriction. There is, however, no clarity concerning the pathways leading to this increased contraction. In this study we elicit and compare maximum contractility of rat aortas under resting conditions in the presence of arsenic and mercury, and delineate pathways mediating this effect. Phenylephrine (PE) induced hypercontraction of 37% and 32% were obtained when isolated aortic segments were exposed to 25 ?M As(III) and 6 nM Hg(II), respectively. Isometric contraction measurements in presence of apocynin, verapamil and sodium nitroprusside indicates that the major causes of increased contraction are reactive oxygen species (ROS) and depletion of nitric oxide (NO). Calcium influx plays a minor role in arsenic and mercury caused hypercontraction. In unexposed aorta, eugenol causes relaxation by inhibiting ROS and elevating NO, linalool by blocking voltage dependent calcium channel (VDCC) and elevating NO, and carvone by blocking calcium influx through VDDC. Since the arsenic and mercury hypercontraction is mediated by increased ROS and depleted NO, we hypothesize that molecules which neutralize ROS or elevate NO will be better ameliorators. In line with this argument, we found eugenol to be the best ameliorator of arsenic and mercury hypercontraction followed by linalool and carvone.
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