ArticleVascular pharmacology
Big ET-1 processing into vasoactive peptides in arteries and veins.
Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Trial
- Association between big endothelin-1 and CHADSJournal of geriatric cardiology : JGC · 2019Article
- Big endothelin-1 as a clinical marker for ventricular tachyarrhythmias in patients with post-infarction left ventricular aneurysm.Anatolian journal of cardiology · 2019Article
- Associations of big endothelin-1 and C-reactive protein in atrial fibrillation.Journal of geriatric cardiology : JGC · 2016Article
- Endothelin.Pharmacological reviews · 2016Review
- Enhanced vascular chymase-dependent conversion of endothelin in the diabetic kidney.Ochsner journal · 2013Article
- Elevated peripheral neutrophils and matrix metalloproteinase 9 as biomarkers of functional outcome following subarachnoid hemorrhage.Translational stroke research · 2011Article
- Functional and molecular characterization of the endothelin system in retinal arterioles.Investigative ophthalmology & visual science · 2009Article
- A comparison of reactive oxygen species metabolism in the rat aorta and vena cava: focus on xanthine oxidase.American journal of physiology. Heart and circulatory physiology · 2008Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The endothelin (ET) peptides are more potent in contracting veins than arteries. The precursor big ET-1 is metabolized by endothelin converting enzyme [ECE; to ET-1 (1-21)], matrix metalloproteases [MMPs; to ET-1 (1-32)] and chymase [to ET-1(1-31)]. We hypothesized that arteries and veins were differently dependent in conversion of big ET-1 to vasoconstrictors. Immunohistochemical, western, zymographic and isometric contractile assays in rat aorta and vena cava were used. Big ET-1 contracted aorta [60+/-17% phenylephrine contraction] but was more efficacious in vena cava [478+/-61% norepinephrine contraction]. ECE and its product ET-1(1-21) were detected in aorta and vena cava, and the ECE inhibitors phosphoramidon and CGS-26393 reduced big ET-1-induced contraction. ET-1 (1-32) contracted aorta and vena cava but inhibition of MMPs with minocycline or GM6001 did not reduce big ET-1-induced contraction; zymography confirmed active tissue MMPs. Aorta and vena cava contracted to the product of chymase, ET-1 (1-31). Chymase was detected in aorta and only weakly in vena cava. Inhibition of chymase (chymostatin, 100 muM) reduced arterial (19% control) but not venous constriction to big ET-1. These results suggest at least one potential significant difference - the role of chymase - in in vitro enzymatic processing of big ET-1 in arteries and veins.
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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.