A novel mechanism of vascular relaxation induced by sodium nitroprusside in the isolated rat aorta

Bonaventura, Daniella; Lunardi, Claure N.; Rodrigues, Gerson Jhonatan; Neto, Mario Abreu Soares; Bendhack, Lusiane Maria

doi:10.1016/j.niox.2008.02.004

Cited by 54 publications

(45 citation statements)

References 30 publications

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“…In isolated aortic rings the endothelium potentiates the relaxation induced by sodium nitroprusside (NO donor), by a mechanism dependent of endothelium Ca 2+ influx with consequent NOS activation, as verified previously [22]. Under reduction, the SNP release NO [22] and cyanide [23] and the compound DETA-NO release just NO and spontaneously [24]. Thus, DETA-NO is a better pharmacological tool to investigate the effect of NO in endothelial cells.…”

Section: Discussionsupporting

confidence: 60%

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Martinelli¹,

Rodrigues²,

Moraes³

et al. 2018

J Pharm Pharm Sci

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-Purpose. In endothelial cells, investigate if the soluble guanylate cyclase (sGC) activation or stimulation is able to potentiate the relaxation in vessels. Methods. Aortic and coronary rings with and without endothelium were placed in a myograph and cumulative concentration-effect curves for DETA-NO or ataciguat were performed. Nitric oxide (NO) were measured by fluorescence or by selective electrode in human umbilical endothelial cells (HUVECs) in response to some treatments, including ataciguat, 8-BrcGMP and A23187. Results. The presence of the endothelium potentiated the relaxation induced by DETA-NO in aortic and coronary rings. In addition, in aortic rings the endothelium potentiated the relaxation induced by ataciguat. In the presence of nitric oxide synthase (NOS) inhibitor, the endothelium effect was abolished to DETA-NO or ataciguat, in both vessels. Ataciguat, 8-Br-cGMP and A23187 were able to induce NO production in HUVECs cells. In the presence of NOS inhibitor, the NO production induced by ataciguat and 8-Br-cGMP was abolished. Conclusions. Our results suggest that in aortic and coronary rings the endothelium potentiates the relaxation induced by activation or stimulation of sGC through a mechanism dependent of NOS activation.

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Section: Discussionsupporting

confidence: 60%

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Martinelli¹,

Rodrigues²,

Moraes³

et al. 2018

J Pharm Pharm Sci

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“…NO can be exogenously supplied to tissues and cells by various NO-generating compounds. The inorganic compound SNP is an agent that releases NO in biologic systems by nonenzymatic and enzymatic mechanisms (Kowaluk et al, 1992;Bonaventura et al, 2008). In our study, SNP-induced cavernosal relaxations were significantly increased in SCD and dNOS 2/2 groups, which were restored to WT values by treatment with compound 4C.…”

Section: Discussionsupporting

confidence: 55%

Beneficial Effect of the Nitric Oxide Donor Compound 3-(1,3-Dioxoisoindolin-2-yl)Benzyl Nitrate on Dysregulated Phosphodiesterase 5, NADPH Oxidase, and Nitrosative Stress in the Sickle Cell Mouse Penis: Implication for Priapism Treatment

Silva

Karakus

Musicki

et al. 2016

J Pharmacol Exp Ther

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Patients with sickle cell disease (SCD) display priapism, and dysregulated nitric oxide (NO) pathway may contribute to this condition. However, current therapies offered for the prevention of priapism in SCD are few. The 3-(1,3-dioxoisoindolin-2-yl)benzyl nitrate (compound 4C) was synthesized through molecular hybridization of hydroxyurea and thalidomide, which displays an NO-donor property. This study aimed to evaluate the effects of compound 4C on functional and molecular alterations of erectile function in murine models that display low NO bioavailability, SCD transgenic mice, and endothelial NO synthase and neuronal NO synthase double gene-deficient (dNOS 2/ ) mice, focusing on the dysregulated NO-cGMP-phosphodiesterase type 5 (PDE5) pathway and oxidative stress in erectile tissue. Wild-type, SCD, and dNOS 2/2 mice were treated with compound 4C (100 mmol/kg/d, 3 weeks). Intracavernosal pressure in anesthetized mice was evaluated. Corpus cavernosum tissue was dissected free and mounted in organ baths. SCD and dNOS 2/2 mice displayed a priapism phenotype, which was reversed by compound 4C treatment. Increased corpus cavernosum relaxant responses to acetylcholine and electrical-field stimulation were reduced by 4C in SCD mice. Likewise, increased sodium nitroprusside-induced relaxant responses were reduced by 4C in cavernosal tissue from SCD and dNOS 2/2 mice. Compound 4C reversed PDE5 protein expression and reduced protein expressions of reactive oxygen species markers, NADPH oxidase subunit gp91 phox , and 3-nitrotyrosine in penises from SCD and dNOS 2/2 mice. In conclusion, 3-week therapy with the NO donor 4C reversed the priapism in murine models that display lower NO bioavailability. NO donor compounds may constitute an additional strategy to prevent priapism in SCD.

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“…In our study, the eŠects of cooling to sodium nitroprusside, which mediates its vasorelaxant eŠects in contractile cells is via nitric oxide released in the vascular smooth cells 34) were also studied, and it was found that the relaxations to this substance were not in‰uenced by cooling and it can therefore be assumed that the ability of the smooth muscle cells to relax to nitrous compounds remains essentially unaltered at lowered temperatures in human umbilical artery. In a previous study, we found the similar result with sodium nitroprusside in calf coronary artery and cardiac vein.…”

Section: Discussionmentioning

confidence: 96%

Role of the Nitric Oxide on Relaxation of the Human Umbilical Artery during Cooling

2011

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In the present study, the eŠects of cooling (to 28°C) on the vasodilatation induced by diazoxide (10 -9 -3×10 -4 M), isoproterenol (10 -9 -3×10 -4 M) and magnesium sulphate (0.1 30 mM) on serotonin-pre-contracted human umbilical artery and the role of nitric oxide in these eŠects were analyzed. Diazoxide, isoproterenol and magnesium produced concentration-dependent relaxation of human umbilical artery precontracted with serotonin (10 -6 M). During cooling, the pIC 50 values and maximal responses to these agents were signiˆcantly lower than at 37°C. Cooling to 28°C in the presence of N G -nitro-L-arginine methyl ester (L-NAME, 10 -4 M) did not modify the eŠects of temperature on diazoxide, isoproterenol and magnesium-induced relaxations. These results suggest that cooling-induced changes of diazoxide, isoproterenol, and magnesium sulphate in human umbilical artery are independent of nitric oxide.

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A novel mechanism of vascular relaxation induced by sodium nitroprusside in the isolated rat aorta

Cited by 54 publications

References 30 publications

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

In Endothelial Cells, the Activation or Stimulation of Soluble Guanylyl Cyclase Induces the Nitric Oxide Production by a Mechanism Dependent of Nitric Oxide Synthase Activation

Beneficial Effect of the Nitric Oxide Donor Compound 3-(1,3-Dioxoisoindolin-2-yl)Benzyl Nitrate on Dysregulated Phosphodiesterase 5, NADPH Oxidase, and Nitrosative Stress in the Sickle Cell Mouse Penis: Implication for Priapism Treatment

Role of the Nitric Oxide on Relaxation of the Human Umbilical Artery during Cooling

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