ArticleNitric oxide : biology and chemistry2012
Effect of chronic sodium nitrite therapy on monocrotaline-induced pulmonary hypertension.
Article in Nitric oxide : biology and chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Therapy for Pulmonary Arterial Hypertension: Glance on Nitric Oxide Pathway.Frontiers in pharmacology · 2021Review
- Preventive effects of nitrate-rich beetroot juice supplementation on monocrotaline-induced pulmonary hypertension in rats.PloS one · 2021Article
- Airway nitrite is increased in extremely preterm infants with bronchopulmonary dysplasia.Respiratory research · 2020Article
- Nutraceuticals in the Treatment of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Review
- Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health.Free radical biology & medicine · 2017Review
- A Brief Overview of Nitric Oxide and Reactive Oxygen Species Signaling in Hypoxia-Induced Pulmonary Hypertension.Advances in experimental medicine and biology · 2017Review
- Soluble guanylate cyclase: a new therapeutic target for pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension.Clinical pharmacology and therapeutics · 2015Review
- Intratracheal administration of cyclooxygenase-1-transduced adipose tissue-derived stem cells ameliorates monocrotaline-induced pulmonary hypertension in rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- Oxidative Stress and Therapeutic Development in Lung Diseases.Journal of pulmonary & respiratory medicine · 2014Article
- New insights into the role of soluble guanylate cyclase in blood pressure regulation.Current opinion in nephrology and hypertension · 2014Review
- Inorganic nitrite supplementation for healthy arterial aging.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Review
- Analysis of responses to the TRPV4 agonist GSK1016790A in the pulmonary vascular bed of the intact-chest rat.American journal of physiology. Heart and circulatory physiology · 2014Article
- Nitrate-nitrite-nitric oxide pathway in pulmonary arterial hypertension therapeutics.Circulation · 2012Article
- Recent publications by ochsner authors.Ochsner journal · 2012Article
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8 authors at 1 institution in 1 country.
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Abstract
Pulmonary hypertension (PH) is a rare disorder that without treatment is progressive and often fatal within 3 years. The treatment of PH involves the use of a diverse group of drugs and lung transplantation. Although nitrite was once thought to be an inactive metabolite of endothelial-derived nitric oxide (NO), there is increasing evidence that nitrite may be useful in the treatment of PH, but the mechanism by which nitrite exerts its beneficial effect remains uncertain. The purpose of this study was to investigate the effect of chronic sodium nitrite treatment in a PH model in the rat. Following induction of PH with a single injection of monocrotaline, 60 mg; daily ip injections of sodium nitrite (3mg/kg) starting on day 14 and continuing for 21 days, resulted in a significantly lower pulmonary arterial pressure on day 35 when compared to values in untreated animals with monocrotaline-induced PH. In monocrotaline-treated rats, daily treatment with ip nitrite injections for 21 days decreased right ventricular mass and pathologic changes in small pulmonary arteries. Nitrite therapy did not change systemic arterial pressure or cardiac output when values were measured on day 35. The decreases in pulmonary arterial pressure in response to iv injections of sodium nitroprusside, sodium nitrite, and BAY 41-8543 were not different in rats with monocrotaline-induced pulmonary hypertension and rats with chronic nitrite therapy when compared to responses in animals in which pulmonary arterial pressure was increased with U46619. These findings are consistent with the hypothesis that the mechanisms that convert nitrite to vasoactive NO, activate soluble guanylyl cyclase and mediate the vasodilator response to NO or an NO derivative are not impaired. The present data are consistent with the results of a previous study in monocrotaline-induced PH in which systemic arterial pressure and cardiac output were not evaluated and are consistent with the hypothesis that nitrite is effective in the treatment of monocrotaline-induced PH in the rodent.
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