Sex differences of endothelial dysfunction markers — nitric oxide synthase and heme oxygenase in rats with 2 type diabetes mellitus
DOI:
https://doi.org/10.21856/j-PEP.2018.4.04Keywords:
type 2 diabetes, sex differences, endothelial dysfunction, nitric oxide synthase, heme oxygenase, ratsAbstract
The effect of type 2 diabetes on the markers of endothelial dysfunction — nitric oxide synthase and heme oxygenase has been studied in rats, depending on sex. It was established that the activity of nitric oxide synthase in the blood vessels of female rats is significantly higher in comparison with males under physiological conditions. Type 2 diabetes leads to the different depression of the nitric oxide synthase activity in the blood vessels of females and males, which eliminates sexual differences in the activity of this enzyme. It was found that in contrast to nitric oxide synthase, the activity of heme oxygenase in vascular homogenate does not depend on the sex of intact animals. Type 2 diabetes leads to more expressive increase in heme oxygenase activity in female blood vessels compared to male rats. We can suppose that a more pronounced elevation of the heme oxygenase activity in case of a decrease the nitric oxide synthase activity is a compensatory mechanism for reducing of endothelial dysfunction in women with type 2 diabetes.
References
Maric-Bilkan C. Clin Sci 2017; 131 (9): 833-846. doi: http://doi.org/10.1042/CS20160998.
Leosdottir M, Willenheimer R, Persson M, Nilsson PM. Cardiovasc Diabetol 2011; 10: 118. doi: http://doi.org/10.1186/1475-2840-10-118.
Williams LJ, Nye BG, Wende AR. Endocrinol Metab (Seoul) 2017; 32 (2): 171-179. doi: http://doi.org/10.3803/EnM.2017.32.2.171.
Odegaard A, Jacobs Jr, Sanchez O. Cardiovasc Diabetol 2016; 15: 51. doi: http://doi.org/10.1186/s12933-016-0369-6.
Stirone C, Boroujerdi A, Duckles SP, Krause DN. Molec Pharmacol 2005; 67 (1): 105-113.
Rahimian R, Chan L, Goel A, et al. Biochem Biophys Res Commun 2004; 322 (2): 373-379.
Hernández I, Delgado JL, Díaz J, et al. Amer J Physiol Regul Integr Comp Physiol 2000; 279 (5): R1599-R1605.
Strehlow K, Rotter S, Wassmann S. Circ Res 2003;93 (2): 170-177.
Marcantoni E, Di Francesco L, Totani L, et al. Prostaglandins Other Lipid Mediat 2012; 98: 122-128. doi: http://doi.org/10.1016/j.prostaglandins.2012.01.006.
Rochette L, Zeller M, Cottin Y, Vergely C. Trends Endocrinol Metab 2018; 29 (2): 74-85. doi: http://doi.org/10.1016/j.tem.2017.11.005.
Chandrakumar L, Bagyánszki M, Oxid Z, et al. Med Cell Longev 2017; 2017 (4): F1158-F1165. doi: http://doi.org/10.1155/2017/1890512.
Failli P, Vannacci A, Di Cesare Mannelli L, et al. Cardiovasc Drugs Ther 2012; 26 (4): 285-292. doi: http://doi.org/10.1007/ s10557-012-6400-6.
Velmurugan GV, Sundaresan NR, Gupta MP, White C. Cardiovascular Res 2013; 100: 143-150. doi: http://doi.org/10.1093/cvr/cvt125.
Rjeznikov OG. Endokrynologija 2003; 8 (1): 142-145.
Lin S, Yang J, Wu G, et al. J Biomed Sci 2010; 17 (1): 46-56. doi: http://doi.org/10.1186/1423-0127-17-S1-S46.
Berger V, Gelger R, Hess J, et al. Amer J Respir Crit Care Med 2001; 163 (6): 1493-1499.
Nowell S, Leakey J, Warren J, et al. J Biol Chem 1998;273 (50): 33342-33346.
Lowry O, Rosenbrought N, Farr A. J Biol Chem 1951;193 (1): 265-270.
Glans S. Mediko-biologicheskaja statistika, Moskva, 1998: 459 p.
Cattaneo MG, Vanetti C, Decimo I, et al. Scientific Reports 2017; 7: 9612-9625. doi: http://doi.org/10.1038/s41598-017-10139-x.
Beleznaia T, Bagia Z. Vascul Pharmacol 2012; 56: 115-117. doi: http://doi.org/10.1016/j.vph.2011.11.003.
Zimmermann K, Baldinger J, Mayerhofer B, et al. Free Radic Biol Med 2015; 88: 417-426. doi: http://doi.org/10.1016/j.freeradbiomed.2015.03.030.
Velmurugan GV, Sundaresan NR, Gupta MP, White C. Cardiovasc Res 2013; 100: 143-150. doi: http://doi.org/10.1093/cvr/cvt125.
K.Niture S, Khatri R, Jaiswal AK. Toxicol Report 2014;66 (8): 36-44. doi: http://doi.org/10.1016/j.toxrep.2017.06.002.
Niture SK, Jain AK, Jaiswal AK. J Cell Science 2009;122: 4452-4464. doi: http://doi.org/10.1242/jcs.058537.