Treatment with sodium nitroprusside improves the endothelial function in aortic rings with endothelial dysfunction
| Autor: | Izabela Pereira Vatanabe, Thiago Francisco De Moraes, Cezar R. Pestana, Gerson Jhonatan Rodrigues, Jorge Oishi, T.C. Buzinari, Heloisa S. Selistre-de-Araujo |
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| Rok vydání: | 2017 |
| Předmět: |
Male
Nitroprusside 0301 basic medicine Cell Survival Vasodilator Agents Pharmaceutical Science Aorta Thoracic In Vitro Techniques 030204 cardiovascular system & hematology Pharmacology Nitric Oxide Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Superoxides Human Umbilical Vein Endothelial Cells medicine Animals Humans Nitric Oxide Donors Rats Wistar Endothelial dysfunction Phenylephrine Antihypertensive Agents Cells Cultured medicine.disease Angiotensin II Hypertension Renovascular 030104 developmental biology chemistry Sodium nitroprusside PubChem Acetylcholine Myograph medicine.drug |
| Zdroj: | European Journal of Pharmaceutical Sciences. 105:144-149 |
| ISSN: | 0928-0987 |
| DOI: | 10.1016/j.ejps.2017.04.022 |
| Popis: | Purpose Verify if sodium nitroprusside (SNP) is able to improve endothelial function and if this effect is independent of nitric oxide (NO) release of the compound. Methods Normotensive (2K) and hypertensive (2K-1C) wistar rats were used. Intact endothelium aortas were placed in a myograph and incubated with SNP: 0.1 nM; 1 nM or 10 nM during 30 min. Cumulative concentration-effect curves for acetylcholine (Ach) were realized to measure the relaxing capacity. Intracellular NO were measured (by DAF-2DA probe) in HUVEC treated with SNP 0.1 nM or DETA/NO 0.1 μM. The detection of intracellular superoxide radical (O 2 •- ) was obtained by using DHE probe. Results Treatment of 2K-1C aortic rings with SNP (0.1; 1.0 and 10 nM) improved endothelium dependent relaxation induced by acetylcholine. This improvement induced by SNP was verified at the concentration of 0.1 nM, which does not release NO, suggesting that this effect was not induced due to NO release by SNP compound. Besides, we show that the cell treatment with 0.1 nM of SNP decreased the fluorescence intensity to DHE in cells stimulated with angiotensin II. These results indicate that SNP decreases the concentration of O 2 •- in HUVEC cells. Conclusions The SNP at a concentration that does not release NO inside the cells is able to attenuate endothelial dysfunction. Drugs and chemicals Acetylcholine (Ach) (PubChem CID:6060); angiotensin II human (Ang II) (PubChem CID: 16211177); diethylenetriamine/nitric oxide (DETA-NO) (PubChem CID 4518); dihydroethidium (DHE) (PubChem CID: 128682); phenylephrine (Phe) (PubChem CID: 5284443); sodium nitroprusside (SNP) (PubChem CID: 11963579); Thiazolyl Blue Tetrazolium Bromide (MTT) (PubChem CID: 64965); 4,5-diaminofluorescein diacetate (DAF-2DA); 4-hidroxy-Tempo (Tempol) (PubChem CID: 137994), were purchased from Sigma–Aldrich (St. Louis, MO, USA). |
| Databáze: | OpenAIRE |
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