ReviewBritish journal of pharmacology2005
Endothelium-dependent contractions in hypertension.
Review in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 279 citations in OpenAlex.
- Trial
- FTO Deficiency Inhibits Vascular Endothelial Cell Apoptosis and Improved Mitophagy in Obesity-Related Hypertension by Enhancing NDRG1 m6A Methylation.Biochemical genetics · 2026Article
- The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- Regional heterogeneity in vascular contractile dysfunction in diabetic mice.Molecular and cellular biochemistry · 2025Article
- Article
- Endothelial cell Orai1 is essential for endothelium-dependent contraction of mouse carotid arteries in normotensive and hypertensive mice.Acta pharmacologica Sinica · 2024Article
- Endothelial Dysfunction under the Scope of Arterial Hypertension, Coronary Heart Disease, and Diabetes Mellitus using the Angioscan.Cardiovascular & hematological agents in medicinal chemistry · 2024Article
- Chronic SIRT1 supplementation in diabetic mice improves endothelial function by suppressing oxidative stress.Cardiovascular research · 2023Article
- A Mathematical Model of Maladaptive Inward Eutrophic Remodeling of Muscular Arteries in Hypertension.Journal of biomechanical engineering · 2023Article
- 7-Hydroxycoumarin Induces Vasorelaxation in Animals with Essential Hypertension: Focus on Potassium Channels and Intracellular CaMolecules (Basel, Switzerland) · 2022Article
- Review
- The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19.International journal of molecular sciences · 2022Review
- TRPC5 is essential in endothelium-dependent contraction of aorta from diet-induced obese mice.Fundamental research · 2022Article
- Nitric Oxide as a Central Molecule in Hypertension: Focus on the Vasorelaxant Activity of New Nitric Oxide Donors.Biology · 2021Review
- An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging.Nature aging · 2021Article
- Berberine: A Review of its Pharmacokinetics Properties and Therapeutic Potentials in Diverse Vascular Diseases.Frontiers in pharmacology · 2021Review
- Endothelial dysfunction in small arteries and early signs of atherosclerosis in ApoE knockout rats.Scientific reports · 2020Article
- Uremic Toxins and Vascular Dysfunction.Toxins · 2020Review
- The Obligatory Role of the Acetylcholine-Induced Endothelium-Dependent Contraction in Hypertension: Can Arachidonic Acid Resolve this Inflammation?Current pharmaceutical design · 2020Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Endothelial cells, under given circumstances, can initiate contraction (constriction) of the vascular smooth muscle cells that surround them. Such endothelium-dependent, acute increases in contractile tone can be due to the withdrawal of the production of nitric oxide, to the production of vasoconstrictor peptides (angiotensin II, endothelin-1), to the formation of oxygen-derived free radicals (superoxide anions) and/or the release of vasoconstrictor metabolites of arachidonic acid. The latter have been termed endothelium-derived contracting factor (EDCF) as they can contribute to moment-to-moment changes in contractile activity of the underlying vascular smooth muscle cells. 2. To judge from animal experiments, EDCF-mediated responses are exacerbated by aging, spontaneous hypertension and diabetes. 3. To judge from human studies, they contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. 4. Since EDCF causes vasoconstriction by activation of the TP-receptors on the vascular smooth muscle cells, selective antagonists at these receptors prevent endothelium-dependent contractions, and curtail the endothelial dysfunction in hypertension and diabetes.
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Registered trials
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.