ArticleBritish journal of pharmacology2011
AVE3085, an enhancer of endothelial nitric oxide synthase, restores endothelial function and reduces blood pressure in spontaneously hypertensive rats.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 48 citations in OpenAlex.
- Advancements in the Research of New Modulators of Nitric Oxide Synthases Activity.International journal of molecular sciences · 2024Review
- Dysfunctional and Dysregulated Nitric Oxide Synthases in Cardiovascular Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2023Review
- Review
- Experimental heart failure models in small animals.Heart failure reviews · 2023Review
- Targeting IRE1α-JNK-c-Jun/AP-1-sEH Signaling Pathway Improves Myocardial and Coronary Endothelial Function Following Global Myocardial Ischemia/Reperfusion.International journal of medical sciences · 2022Article
- New Therapeutic Implications of Endothelial Nitric Oxide Synthase (eNOS) Function/Dysfunction in Cardiovascular Disease.International journal of molecular sciences · 2019Review
- Thrombosis and Vascular Inflammation in Diabetes: Mechanisms and Potential Therapeutic Targets.Frontiers in cardiovascular medicine · 2018Review
- Attenuation of blood pressure in spontaneously hypertensive rats by acupuncture was associated with reduction oxidative stress and improvement from endothelial dysfunction.Chinese medicine · 2016Article
- Endothelial Gata5 transcription factor regulates blood pressure.Nature communications · 2015Article
- Vascular endothelial dysfunction and pharmacological treatment.World journal of cardiology · 2015Review
- Suxiao jiuxin pill induces potent relaxation and inhibition on contraction in human artery and the mechanism.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- Endothelial dysfunction in experimental models of arterial hypertension: cause or consequence?BioMed research international · 2014Review
- Defensive effect of natrium diethyldithiocarbamate trihydrate (NDDCT) and lisinopril in DOCA-salt hypertension-induced vascular dementia in rats.Psychopharmacology · 2012Article
- Targeting endothelial dysfunction in vascular complications associated with diabetes.International journal of vascular medicine · 2012Article
- Highly Diluted Antibodies to eNOS Restore Endothelium Function in Aortic Rings From Hypertensive Rats.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeNitric oxide (NO) plays an important role in endothelial function, and impaired NO production is involved in hypertension. Therefore, compounds that regulate endothelial NO synthase (eNOS) may be of therapeutic benefit. A novel, low molecular weight compound AVE3085 is a recently developed compound with the ability to enhance eNOS transcription. The present study investigated the effects of AVE3085 in endothelial dysfunction associated with hypertension. EXPERIMENTAL APPROACH: Spontaneously hypertensive rats (SHRs) were treated with AVE 3085 (10 mg·kg·day(-1) , orally) for 4 weeks. Isometric force measurement was performed on rings of isolated aortae in organ baths. Protein expression of eNOS, phosphorylated-eNOS and nitrotyrosine in the aortae were examined by Western blotting. mRNA for eNOS in rat aortae were examined by reverse-transcriptase polymerase chain reaction (RT-PCR). KEY
resultsAVE3085 greatly improved endothelium-dependent relaxations in the aortae of SHRs. This functional change was accompanied by up-regulated expression of eNOS protein and mRNA, enhanced eNOS phosphorylation and decreased formation of nitrotyrosine. Furthermore, AVE3085 treatment reduced the blood pressure in SHR without affecting that of hypertensive eNOS(-/-) mice. CONCLUSIONS AND IMPLICATIONS: The eNOS-transcription enhancer AVE3085 restored impaired endothelial function in a hypertensive model. The present study provides a solid basis for the potential development of eNOS-targeting drugs to restore down-regulated eNOS, as a new strategy in hypertension.
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