ArticleHeart and vessels2014
Diverse effects of prostaglandin E₂ on vascular contractility.
Article in Heart and vessels, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
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- Cytoprotection as a Unifying Strategy for Hemorrhage and Thrombosis: The Role of BPC 157 and Related Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Combining machine learning with external validation to explore necroptosis and immune response in moyamoya disease.BMC immunology · 2025Article
- Review
- Associations of E-proteinoid 3 receptor genetic polymorphisms with salt sensitivity, longitudinal blood pressure changes, and hypertension incidence in Chinese adults.Journal of clinical hypertension (Greenwich, Conn.) · 2024Article
- Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?Journal of neuroinflammation · 2024Review
- Article
- The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice.International journal of molecular sciences · 2021Article
- Inflammatory Effects ofToxins · 2021Review
- Multiple roles of the PGE2 -EP receptor signal in vascular permeability.British journal of pharmacology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E₂ (PGE₂) is a major prostanoid produced under inflammatory situations. There have been controversial reports showing contractile or relaxant effect of PGE₂ on vascular tone in various types of blood vessels. Thus, it is still elusive whether and how PGE₂ modulates vascular tone. We here assessed the effects of PGE₂ on vascular contractility using different types of vasculatures isolated form rat. In endothelium-denuded aortas and mesenteric arteries, PGE₂ (1 nM-10 μM) concentration-dependently enhanced the contraction elicited by K(+) (35.4 mM) or norepinephrine (10 nM). In pulmonary arteries, PGE₂ did not alter the both-induced contraction. Tail arteries were relaxed by a low dose of PGE₂ (1-100 nM), but this response shifted to contraction by the higher dose of PGE₂ (300 nM-10 μM). There are four types of PGE₂ receptors EP1-4. RT-PCR showed that aortas and mesenteric arteries abundantly expressed EP3, while tail arteries abundantly expressed EP4. We next revealed that selective EP3 agonism enhanced the contraction in mesenteric arteries, whereas EP4 agonism induced relaxation in tail arteries. Taken together, PGE₂ causes different contractile responses depending on the type of vascular bed. This phenomenon may be due to the difference in expression pattern and activity of EP receptors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.