Treatment with sodium nitroprusside improves the endothelial function in aortic rings with endothelial dysfunction

• Published in: European journal of pharmaceutical sciences Vol. 105; pp. 144 - 149
• Main Authors: Buzinari, Tereza Cristina, Oishi, Jorge Camargo, De Moraes, Thiago Francisco, Vatanabe, Izabela Pereira, Selistre-de-Araújo, Heloisa Sobreiro, Pestana, Cezar Rangel, Rodrigues, Gerson Jhonatan
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.07.2017
• Subjects: Animals; Antihypertensive Agents - pharmacology; Aorta, Thoracic - drug effects; Aorta, Thoracic - physiology; Cell Survival - drug effects; Cells, Cultured; Endothelial dysfunction; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Hypertension, Renovascular - metabolism; Hypertension, Renovascular - physiopathology; In Vitro Techniques; Male; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Donors - pharmacology; Nitroprusside - pharmacology; Rats, Wistar; Sodium nitroprusside; Superoxide; Superoxides - metabolism; Vasodilator Agents - pharmacology; Endothelial dysfunction; Sodium nitroprusside; Superoxide; Nitric oxide
• ISSN: 0928-0987; 1879-0720
• DOI: 10.1016/j.ejps.2017.04.022

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. Normotensive (2K) and hypertensive (2K-1C) wistar rats were used. Intact endothelium aortas were placed in a myograph and incubated with SNP: 0.1nM; 1nM or 10nM during 30min. 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 0.1nM or DETA/NO 0.1μM. The detection of intracellular superoxide radical (O2•-) was obtained by using DHE probe. Treatment of 2K-1C aortic rings with SNP (0.1; 1.0 and 10nM) improved endothelium dependent relaxation induced by acetylcholine. This improvement induced by SNP was verified at the concentration of 0.1nM, 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 0.1nM of SNP decreased the fluorescence intensity to DHE in cells stimulated with angiotensin II. These results indicate that SNP decreases the concentration of O2•- in HUVEC cells. The SNP at a concentration that does not release NO inside the cells is able to attenuate endothelial dysfunction. 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).