Orally administered sodium nitrite prevents the increased α-1 adrenergic vasoconstriction induced by hypertension and promotes the S-nitrosylation of calcium/calmodulin-dependent protein kinase II

Oliveira-Paula, Gustavo H.; Batista, Rose I.M.; Stransky, Stephanie; Tella, Sandra C.; Ferreira, Graziele C.; Portella, Rafael de Lima; Pinheiro, Lucas C.; Damacena-Angelis, Célio; Riascos-Bernal, Dario F.; Sibinga, Nicholas E.S.; Tanus‐Santos, Jose E.

doi:10.1016/j.bcp.2023.115571

Cited by 2 publications

(3 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have suggested that sodium nitrite-derived NO orally administered could attenuate arterial hypertension in animals [ 12 , 19 , 20 , 36 , 37 , 38 ] and humans [ 39 ], including pregnancy hypertension [ 6 , 7 ]. It has also been demonstrated that ionized nitrite is recycled back to NO, thus providing an alternative to restore NO levels independently of NO synthesis by the endothelium [ 12 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

“…The rats treated with sodium nitrite (Preg + Nitrite and RUPP + Nitrite groups) received a dose of 15 mg/kg/day (equivalent to 0.217 mmol/kg) daily, via gavage, from the 14th gestational day until the end of pregnancy, as previously demonstrated that this dose exerted antihypertensive effects in several experimental models of hypertension [ 6 , 36 , 53 , 54 ]. The Norm-Preg and RUPP groups received 0.9% saline solution daily, by gavage, from the 14th gestational day until the end of pregnancy, as schematically represented in the Figure 8 .…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Sodium Nitrite Attenuates Reduced Activity of Vascular Matrix Metalloproteinase-2 and Vascular Hyper-Reactivity and Increased Systolic Blood Pressure Induced by the Placental Ischemia Model of Preeclampsia in Anesthetized Rats

Martins,

da Silva,

Rodrigues

et al. 2023

IJMS

View full text Add to dashboard Cite

Preeclampsia is a maternal hypertension disorder associated with vascular dysfunction and fetal and placental growth restrictions. Placental ischemia is suggested as the primary trigger of preeclampsia-associated impairments of both endothelium-derived nitric oxide (NO) and the vascular activity of extracellular matrix metalloproteinase-2 (MMP-2). Reduced uteroplacental perfusion pressure (RUPP) is a placental ischemia model of preeclampsia. Reduction of sodium nitrite to NO may occur during ischemic conditions. However, sodium nitrite effects in the RUPP model of preeclampsia have not yet been investigated. Pregnant rats were divided into four groups: normotensive pregnant rats (Norm-Preg), pregnant rats treated with sodium nitrite (Preg + Nitrite), preeclamptic rats (RUPP), and preeclamptic rats treated with sodium nitrite (RUPP + Nitrite). Maternal blood pressure and fetal and placental parameters were recorded. Vascular function, circulating NO metabolites, and the gelatinolytic activity of vascular MMP-2 were also examined. Sodium nitrite attenuates increased blood pressure, prevents fetal and placental weight loss, counteracts vascular hyper-reactivity, and partially restores NO metabolites and MMP-2 activity. In conclusion, sodium nitrite reduction to NO may occur during RUPP-induced placental ischemia, thereby attenuating increased blood pressure, fetal and placental growth restriction, and vascular hyper-reactivity associated with preeclampsia and possibly restoring NO and MMP-2 activity, which underlie the blood pressure-lowering effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Sodium Nitrite Attenuates Reduced Activity of Vascular Matrix Metalloproteinase-2 and Vascular Hyper-Reactivity and Increased Systolic Blood Pressure Induced by the Placental Ischemia Model of Preeclampsia in Anesthetized Rats

Martins,

da Silva,

Rodrigues

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…This observation might be linked to changes in the redox environment of the stomach, which affect nitrosation reactions. Indeed, the hypotensive responses of nitrate and nitrite were associated with increased plasma levels of S-nitrosothiols and vascular S-nitrosation of pharmacological targets involved in blood pressure regulation [ 86 , 87 ].…”

Section: Dietary Nitrite and Nitrate Enhance Gastric Nitrosothiol For...mentioning

confidence: 99%

Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases

Silva-Cunha,

Lacchini,

Tanus-Santos

2024

Antioxidants

Self Cite

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) are often associated with impaired nitric oxide (NO) bioavailability, a critical pathophysiological alteration in CVDs and an important target for therapeutic interventions. Recent studies have revealed the potential of inorganic nitrite and nitrate as sources of NO, offering promising alternatives for managing various cardiovascular conditions. It is now becoming clear that taking advantage of enzymatic pathways involved in nitrite reduction to NO is very relevant in new therapeutics. However, recent studies have shown that nitrite may be bioactivated in the acidic gastric environment, where nitrite generates NO and a variety of S-nitrosating compounds that result in increased circulating S-nitrosothiol concentrations and S-nitrosation of tissue pharmacological targets. Moreover, transnitrosation reactions may further nitrosate other targets, resulting in improved cardiovascular function in patients with CVDs. In this review, we comprehensively address the mechanisms and relevant effects of nitrate and nitrite-stimulated gastric S-nitrosothiol formation that may promote S-nitrosation of pharmacological targets in various CVDs. Recently identified interfering factors that may inhibit these mechanisms and prevent the beneficial responses to nitrate and nitrite therapy were also taken into consideration.

show abstract

Orally administered sodium nitrite prevents the increased α-1 adrenergic vasoconstriction induced by hypertension and promotes the S-nitrosylation of calcium/calmodulin-dependent protein kinase II

Cited by 2 publications

References 78 publications

Sodium Nitrite Attenuates Reduced Activity of Vascular Matrix Metalloproteinase-2 and Vascular Hyper-Reactivity and Increased Systolic Blood Pressure Induced by the Placental Ischemia Model of Preeclampsia in Anesthetized Rats

Sodium Nitrite Attenuates Reduced Activity of Vascular Matrix Metalloproteinase-2 and Vascular Hyper-Reactivity and Increased Systolic Blood Pressure Induced by the Placental Ischemia Model of Preeclampsia in Anesthetized Rats

Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases

Contact Info

Product

Resources

About