Effect of MnSOD (E. coli) on the relaxation caused by sodium nitroprusside on isolated rat renal artery

• Main Authors: MIHAJLO B. SPASIC, MILICA PROSTRAN, SRDJAN MILETIC, SNEZANA SPASIC, ZORANA ORESCANIN, SLOBODAN R. MILOVANOVIC
• Format: Article
• Language: English
• Published: Serbian Chemical Society 2004-11-01
• Series: Journal of the Serbian Chemical Society
• Subjects: sodium nitroprusside; manganese superoxide dismutase; renal artery; spontaneously hypertensive rats
• Online Access: http://www.shd.org.yu/HtDocs/SHD/Vol69/No11/V69-No11-17.pdf

In this study the molecular foundation of nitric oxide induced relaxation of arteries, with or without endothelium, of normotensive and spontanously hypertensive rats was re-examined. With this purpose in mind, the effects of the nitric oxide donor sodium nitroprusside (NaNP), with and without manganese containing superoxide dismutase (MnSOD E.C. 1.15.1.1.), on rat renal artery relaxation was strudied. The results show that the relaxation effect of NaNP is two times higher in normotensive, compared to spontaneously hypertensive rats. Similar differences exist in the relaxation effects of NaNP on isolated renal arteries without endothelium, indicating that besides the difference in the function of an endothelium, concerning basal NO production in normotensive and hypertensive rats, there is a difference with respect to NO relaxation in the smooth muscle that is induced by hypertension. MnSOD decreased the relaxation effect of NaNP in all the examined renal arteries, more in normotensive than in hypertensive ones regardless of the presence of an endothelium. These results show that MnSOD, by modifying the chemical versatility of NO into redox active forms - nitrosonium (NO+) and nitroxyl (NO-), produces different relaxation effects in normotensive and hypertensive arteries of rats, with or without an endothelium, potentiating the role of nitroxyl induced relaxation in sponteneously hypertensive rats. The results prove the need for the synthesis of complex NO donors, as the mechanisms of artery relaxation are different due to an endothel and smooth mouscle changes in hypertensive, as compared to normotensive rats.