ArticleMenopause (New York, N.Y.)2011
Neuronal nitric oxide synthase inhibition improves diastolic function and reduces oxidative stress in ovariectomized mRen2.Lewis rats.
Article in Menopause (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Targeting estrogen receptor signaling for treating heart failure.Heart failure reviews · 2024Review
- Hypertension after the Menopause: What Can We Learn from Experimental Studies?Physiological research · 2023Review
- Sex and the G Protein-Coupled Estrogen Receptor Impact Vascular Stiffness.Hypertension (Dallas, Tex. : 1979) · 2021Article
- The Role of Estrogen Receptors in Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Connecting sex differences, estrogen signaling, and microRNAs in cardiac fibrosis.Journal of molecular medicine (Berlin, Germany) · 2019Review
- G protein-coupled estrogen receptor (GPER) deficiency induces cardiac remodeling through oxidative stress.Translational research : the journal of laboratory and clinical medicine · 2018Article
- Effect of Age, Estrogen Status, and Late-Life GPER Activation on Cardiac Structure and Function in the Fischer344×Brown Norway Female Rat.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017Article
- Acute ascorbic acid infusion increases left ventricular diastolic function in postmenopausal women.Maturitas · 2016Article
- Role of estrogen in diastolic dysfunction.American journal of physiology. Heart and circulatory physiology · 2014Review
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Estrogen therapy, independent of timing, improves cardiac structure and function in oophorectomized mRen2.Lewis rats.Menopause (New York, N.Y.) · 2013Article
- Characterization of the cardiac renin angiotensin system in oophorectomized and estrogen-replete mRen2.Lewis rats.PloS one · 2013Article
- Amelioration of renal injury and oxidative stress by the nNOS inhibitor L-VNIO in the salt-sensitive mRen2.Lewis congenic rat.Journal of cardiovascular pharmacology · 2012Article
- Activation of GPR30 attenuates diastolic dysfunction and left ventricle remodelling in oophorectomized mRen2.Lewis rats.Cardiovascular research · 2012Article
- Testosterone deficiency accelerates neuronal and vascular aging of SAMP8 mice: protective role of eNOS and SIRT1.PloS one · 2012Article
- Tetrahydrobiopterin restores diastolic function and attenuates superoxide production in ovariectomized mRen2.Lewis rats.Endocrinology · 2011Article
- Changes in cardiac heparan sulfate proteoglycan expression and streptozotocin-induced diastolic dysfunction in rats.Cardiovascular diabetology · 2011Article
- Associations of plasma phospholipid omega-6 and omega-3 polyunsaturated Fatty Acid levels and MRI measures of cardiovascular structure and function: the multiethnic study of atherosclerosis.Journal of nutrition and metabolism · 2011Article
- The Role of Estrogen in Cardiac Metabolism and Diastolic Function.Methodist DeBakey cardiovascular journalReview
- Blunting of cardioprotective actions of estrogen in female rodent heart linked to altered expression of cardiac tissue chymase and ACE2.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveThe loss of estrogen in mRen2.Lewis rats leads to an exacerbation of diastolic dysfunction. Because specific neuronal nitric oxide synthase (nNOS) inhibition reverses renal damage in the same model, we assessed the effects of inhibiting neuronal nitric oxide on diastolic function, left ventricular remodeling, and the components of the cardiac nitric oxide system in ovariectomized (OVX) and sham-operated mRen2.Lewis rats treated with N5-(1-imino-3-butenyl)-L-ornithine (L-VNIO; 0.5 mg/kg per day for 28 d) or vehicle (saline).
methodsFemale mRen2.Lewis rats underwent either bilateral oophorectomy (OVX; n = 15) or sham operation (or surgical procedure) (sham; n = 19) at 4 weeks of age. Beginning at 11 weeks of age, the rats were randomized to receive either L-VNIO or vehicle.
resultsThe surgical loss of ovarian hormones, particularly estrogen, led to exacerbated hypertension, impaired myocardial relaxation, diminished diastolic compliance, increased perivascular fibrosis, and increased relative wall thickness. The cardiac tetrahydrobiopterin-to-dihydrobiopterin levels were lower among OVX rats compared with sham-operated rats, and this altered cardiac biopterin profile was associated with enhanced myocardial superoxide production and decreased nitric oxide release. L-VNIO decreased myocardial reactive oxygen species production, increased nitrite concentrations, attenuated cardiac remodeling, and improved diastolic function.
conclusionsImpaired relaxation, diastolic stiffness, and cardiac remodeling were found among OVX mRen2.Lewis rats. A possible mechanism for this unfavorable cardiac phenotype may have resulted from a deficiency in available tetrahydrobiopterin and subsequent increase in nNOS-derived superoxide and reduction in nitric oxide synthase metabolites within the heart. Selective nNOS inhibition with L-VNIO attenuated cardiac superoxide production and limited remodeling, leading to improved diastolic function in OVX mRen2.Lewis rats.
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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.