ReviewBritish journal of pharmacology2009
Endothelium-dependent contractions and endothelial dysfunction in human hypertension.
Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 251 citations in OpenAlex.
- The role of cyclo-oxygenase-1 in high-salt diet-induced microvascular dysfunction in humans.The Journal of physiology · 2015Trial
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- The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.Electrolyte & blood pressure : E & BP · 2026Review
- Construction and validation of the risk assessment scale for deep vein thrombosis in high altitude plateau areas.Frontiers in medicine · 2026Article
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- Heart failure and microvascular dysfunction: an in-depth review of mechanisms, diagnostic strategies, and innovative therapies.Annals of medicine and surgery (2012) · 2025Review
- Acacetin as a natural cardiovascular therapeutic: mechanisms and preclinical evidence.Frontiers in pharmacology · 2025Review
- Shear Stress-Induced AMP-Activated Protein Kinase Modulation in Endothelial Cells: Its Role in Metabolic Adaptions and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Review Article on Molecular Mechanism of Regulation of Hypertension by Macro-elements (Na, K, Ca and Mg), Micro-elements/Trace Metals (Zn and Cu) and Toxic Elements (Pb and As).Biological trace element research · 2024Review
- Arsenic Exposure-Related Hypertension in Bangladesh and Reduced Circulating Nitric Oxide Bioavailability.Environmental health perspectives · 2024Article
- The Renin-Angiotensin System and Cardiovascular-Kidney-Metabolic Syndrome: Focus on Early-Life Programming.International journal of molecular sciences · 2024Review
- New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications.International journal of molecular sciences · 2024Review
- Cardioprotective Effects of Exercise: The Role of Irisin and Exosome.Current vascular pharmacology · 2024Review
- Platelet Cyclic GMP Levels Are Reduced in Patients with Primary Aldosteronism.Journal of clinical medicine · 2023Article
- Irisin Regulates Cardiac Responses to Exercise in Health and Diseases: a Narrative Review.Journal of cardiovascular translational research · 2023Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Does hyperglycemia affect arginine metabolites in critically ill patients? A prospective cohort and in vitro study.Diabetology & metabolic syndrome · 2023Article
- Mechanisms by which statins protect endothelial cells from radiation-induced injury in the carotid artery.Frontiers in cardiovascular medicine · 2023Article
- Role of curcumin in ameliorating hypertension and associated conditions: a mechanistic insight.Molecular and cellular biochemistry · 2022Review
- Review
40 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endothelium is a crucial regulator of vascular physiology, producing in healthy conditions several substances with a potent antiatherosclerotic properties. Accordingly, the presence of endothelial dysfunction is associated with subclinical atherosclerosis and with an increased future risk of cardiovascular events. A large body of evidence supports the fundamental role of nitric oxide (NO) as the main endothelium-derived relaxing factor. However, in the presence of pathological conditions, such as hypertension, endothelial cells, in response to a number of agents and physical stimuli, become also a source of endothelium-derived contracting factors (EDCFs), including endothelins and angiotensin II and particularly cyclooxygenase-derived prostanoids and superoxide anions. These latter were at first identified as responsible for impaired endothelium-dependent vasodilation in patients with essential hypertension. However, cyclooxygenase-dependent EDCFs production is characteristic of the aging process, and essential hypertension seems to only anticipate the phenomenon. It is worth noting that both in aging and hypertension EDCF production is associated with a parallel decrease in NO availability, suggesting that this substance could be oxygen free radicals themselves. Accordingly, in hypertension both indomethacin, a cyclooxygenase inhibitor, and vitamin C, an antioxidant, increase the vasodilation to acetylcholine by restoring NO availability. In conclusion, hypertension is characterized by a decline in endothelial function, associated with a progressive decrease in NO bioavailability and increase in the production of EDCF. The mechanisms that regulate the balance between NO and EDCF, and the processes transforming the endothelium from a protective organ to a source of vasoconstrictor, proaggregatory and promitogenic mediators remain to be determined.
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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 Socratic graph.