ArticleJournal of the American Heart Association2017
Angiotensin II Receptor-Neprilysin Inhibitor Sacubitril/Valsartan Improves Endothelial Dysfunction in Spontaneously Hypertensive Rats.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Sacubitril/Valsartan Ameliorates Inflammation and Oxidative Stress in Hypertensive Heart Disease by Upregulating CAMKK2 Protein and Modulating the AMPK/AKT/GSK-3β Axis.The Kaohsiung journal of medical sciences · 2026Article
- Vascular function in women with heart failure with preserved ejection fraction: a mismatch beyond diastole.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Determining optimal pretreatment in cardiac surgery: an experimental study.General thoracic and cardiovascular surgery · 2025Article
- Article
- Divergent Electrophysiologic Effects of Sacubitril in Digitalis- and Pinacidil-Related Shortened Repolarization: Experimental Evidence for Harmful Effects of Digitalis Glycosides.Pharmaceutics · 2025Article
- Possible role of LCZ696 in atherosclerosis: new inroads and perspective.Molecular and cellular biochemistry · 2024Review
- Review
- Endothelium-Derived Relaxing Factors and Endothelial Function: A Systematic Review.Biomedicines · 2022Review
- Cardiac and Vascular Remodeling After 6 Months of Therapy With Sacubitril/Valsartan: Mechanistic Insights From Advanced Echocardiographic Analysis.Frontiers in cardiovascular medicine · 2022Article
- Study of endothelial function and vascular stiffness in patients affected by dilated cardiomyopathy on treatment with sacubitril/valsartan.American journal of cardiovascular disease · 2022Article
- Association of KATP Gene Polymorphisms with Dyslipidemia and Ischemic Stroke Risks Among Hypertensive Patients in South China.Journal of molecular neuroscience : MN · 2021Article
- Article
- Angiotensin Receptor Blocker and Neprilysin Inhibitor Suppresses Cardiac Dysfunction by Accelerating Myocardial Angiogenesis in Apolipoprotein E-Knockout Mice Fed a High-Fat Diet.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2021Article
- ATP-sensitive potassium channels gene polymorphism rs1799858 affects the risk of macro-/micro-vascular arteriosclerotic event in patients with increased low-density lipoprotein cholesterol levels.Lipids in health and disease · 2020Article
- Article
- Dual Angiotensin Receptor and Neprilysin Inhibitor Ameliorates Portal Hypertension in Portal Hypertensive Rats.Pharmaceutics · 2020Article
- Strain-selective efficacy of sacubitril/valsartan on carotid fibrosis in response to injury in two inbred mouse strains.British journal of pharmacology · 2019Article
- Endothelium-Dependent Hyperpolarization (EDH) in Diabetes: Mechanistic Insights and Therapeutic Implications.International journal of molecular sciences · 2019Review
- ARNi: A Novel Approach to Counteract Cardiovascular Diseases.International journal of molecular sciences · 2019Review
- Neprilysin Inhibitor-Angiotensin II Receptor Blocker Combination Therapy (Sacubitril/valsartan) Suppresses Atherosclerotic Plaque Formation and Inhibits Inflammation in Apolipoprotein E- Deficient Mice.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe have previously demonstrated that antihypertensive treatment with renin-angiotensin system inhibitors restores the impaired endothelium-dependent hyperpolarization (EDH)-mediated responses in spontaneously hypertensive rats (SHRs). Herein, we investigated whether the angiotensin II receptor-neprilysin inhibitor sacubitril/valsartan (LCZ696) would improve reduced EDH-mediated responses and whether LCZ696 would exert additional effects on endothelium-dependent and endothelium-independent vasorelaxation compared with an angiotensin II type 1 receptor blocker alone during hypertension. METHODS AND
resultsSHRs were treated for 3 months with either LCZ696 or valsartan, from the age of 8 to 11 months. Age-matched, untreated SHRs and Wistar-Kyoto rats served as controls. Membrane potentials and contractile responses were recorded from the isolated superior mesenteric arteries. Acetylcholine-induced, EDH-mediated responses were impaired in untreated SHRs compared with Wistar-Kyoto rats. EDH-mediated responses were similarly improved in the LCZ696- and valsartan-treated SHRs. No difference was observed in acetylcholine-induced, nitric oxide-mediated relaxations among the 4 groups. Endothelium-independent relaxations in response to a nitric oxide donor, sodium nitroprusside, and those to levcromakalim, an ATP-sensitive K
conclusionsLCZ696 appears to be as effective as valsartan in improving the impaired EDH-mediated responses during hypertension. LCZ696 and valsartan exert similar beneficial effects on endothelium-independent relaxation via enhanced sensitivity of the ATP-sensitive K
Indexed as
Identifiers
What OpenQuestion holds
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.