ArticleNitric oxide : biology and chemistry2019
Exercise training augments neuronal nitric oxide synthase dimerization in the paraventricular nucleus of rats with chronic heart failure.
Article in Nitric oxide : biology and chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 13 citations in OpenAlex.
- Dapagliflozin lowers blood pressure via regulating the sympathetic neural activity in the paraventricular nucleus of hypothalamus in normal mice.Frontiers in endocrinology · 2026Article
- Potential Mechanisms of Exercise-Mediated Ferroptosis Regulation in Central Nervous System Diseases.Molecular neurobiology · 2025Review
- Degradation of nNOS in the PVN of Rats With Heart Failure: Role of CHIP.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Aerobic Exercise Activates Fibroblast Growth Factor 21 and Alleviates Cardiac Ischemia/Reperfusion-induced Neuronal Oxidative Stress and Ferroptosis in Paraventricular Nucleus.Molecular neurobiology · 2025Article
- The Role and Underlying Mechanisms of Exercise in Heart Failure.Reviews in cardiovascular medicine · 2024Review
- Exercise in treatment-resistant hypertension. A natural neuromodulation therapy?Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Article
- A Critical Role for the Paraventricular Nucleus of the Hypothalamus in the Regulation of the Volume Reflex in Normal and Various Cardiovascular Disease States.Current hypertension reports · 2022Review
- Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction.Arquivos brasileiros de cardiologia · 2021Article
- MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
- GLP-1 mediated diuresis and natriuresis are blunted in heart failure and restored by selective afferent renal denervation.Cardiovascular diabetology · 2020Article
- The Beneficial Role of Exercise Training for Myocardial Infarction Treatment in Elderly.Frontiers in physiology · 2020Review
- Central angiotensin II-Protein inhibitor of neuronal nitric oxide synthase (PIN) axis contribute to neurogenic hypertension.Nitric oxide : biology and chemistry · 2020Article
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5 authors at 1 institution in 1 country.
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Abstract
Exercise training (ExT) is an established non-pharmacological therapy that improves the health and quality of life in patients with chronic heart failure (CHF). Exaggerated sympathetic drive characterizes CHF due to an imbalance of the autonomic nervous system. Neuronal nitric oxide synthase (nNOS) in the paraventricular nucleus (PVN) produce nitric oxide (NO•), which is known to regulate the sympathetic tone. Previously we have shown that during CHF, the catalytically active dimeric form of nNOS is significantly decreased with a concurrent increase in protein inhibitor of nNOS (PIN) expression, a protein that dissociates dimeric nNOS to monomers and facilitates its degradation. Dimerization of nNOS also requires (6R)-5,6,7,8-tetrahydrobiopterin (BH4) for stability and activity. Previously, we have shown that ExT improves NO-mediated sympathetic inhibition in the PVN; however, the molecular mechanism remains elusive. We hypothesized; ExT restores the sympathetic drive by increasing the levels and catalytically active form of nNOS by abrogating changes in the PIN in the PVN of CHF rats. CHF was induced in adult male Sprague-Dawley rats by coronary artery ligation, which reliably mimics CHF in patients with myocardial infarction. After 4 weeks of surgery, Sham and CHF rats were subjected to 3 weeks of progressive treadmill exercise. ExT significantly (p < 0.05) decreased PIN expression and increased dimer/monomer ratio of nNOS in the PVN of rats with CHF. Moreover, we found decreased GTP cyclohydrolase 1(GCH1) expression: a rate-limiting enzyme for BH4 biosynthesis in the PVN of CHF rats suggesting that perhaps reduced BH4 availability may also contribute to decreased nNOS dimers. Interestingly, CHF induced decrease in GCH1 expression was increased with ExT. Our findings revealed that ExT rectified decreased PIN and GCH1 expression and increased dimer/monomer ratio of nNOS in the PVN, which may lead to increase NO• bioavailability resulting in amelioration of activated sympathetic drive during CHF.
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