TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milutinovic, D. V.
AU  - Macut, D.
AU  - Stanišić, Jelena
AU  - Nikolić, M.
AU  - Bozic-Antic, I.
AU  - Rodaljevic, S.
AU  - Bjekic-Macut, J.
AU  - Matić, Gordana
AU  - Korićanac, Goran
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/553
AB  - Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone
VL  - 123
IS  - 5
SP  - 303
EP  - 307
DO  - 10.1055/s-0035-1548929
ER  - 

@article{
author = "Tepavčević, Snežana and Milutinovic, D. V. and Macut, D. and Stanišić, Jelena and Nikolić, M. and Bozic-Antic, I. and Rodaljevic, S. and Bjekic-Macut, J. and Matić, Gordana and Korićanac, Goran",
year = "2015",
abstract = "Nitric oxide synthases (NOSs) and Na+/K+-ATPase are enzymes essential for regular functioning of the heart. Since both enzymes are under insulin and androgen regulation and since insulin action and androgen level were disturbed in polycystic ovary syndrome (PCOS), we hypothesized that cardiac nitric oxide (NO) production and sodium/potassium transport would be deteriorated in PCOS. To test our hypothesis we introduced animal model of PCOS based on dihydrotestosterone (DHT) treatment of female Wistar rats and analyzed protein expression, phosphorylation or subcellular localization of endothelial NOS (eNOS), inducible NOS (iNOS) and alpha subunits of Na+/K+-ATPase in the heart. Obtained results indicate that DHT treatment significantly decreased cardiac eNOS protein level and activating phosphorylation at serine 1177, while inhibitory phosphorylation at threonine 495 was increased. In contrast to expression of eNOS, iNOS protein level in the heart of DHT-treated rats was significantly elevated. Furthermore, cardiac protein level of alpha 1 subunit of the ATPase, as well as its plasma membrane content, were decreased in rats with PCOS. In line with this, alpha 2 subunit protein level in fraction of plasma membranes was also significantly below control level. In conclusion, DHT treatment impaired effectiveness of NOSs and Na+/K+-ATPase in the female rat heart. Regarding the importance of NO production and sodium/potassium transport in the cardiac contraction and blood flow regulation, it implicates strong consequences of PCOS for heart functioning.",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone",
volume = "123",
number = "5",
pages = "303-307",
doi = "10.1055/s-0035-1548929"
}

Tepavčević, S., Milutinovic, D. V., Macut, D., Stanišić, J., Nikolić, M., Bozic-Antic, I., Rodaljevic, S., Bjekic-Macut, J., Matić, G.,& Korićanac, G.. (2015). Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone. in Experimental and Clinical Endocrinology and Diabetes, 123(5), 303-307.
https://doi.org/10.1055/s-0035-1548929

Tepavčević S, Milutinovic DV, Macut D, Stanišić J, Nikolić M, Bozic-Antic I, Rodaljevic S, Bjekic-Macut J, Matić G, Korićanac G. Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone. in Experimental and Clinical Endocrinology and Diabetes. 2015;123(5):303-307.
doi:10.1055/s-0035-1548929 .

Tepavčević, Snežana, Milutinovic, D. V., Macut, D., Stanišić, Jelena, Nikolić, M., Bozic-Antic, I., Rodaljevic, S., Bjekic-Macut, J., Matić, Gordana, Korićanac, Goran, "Cardiac Nitric Oxide Synthases and Na+/K+-ATPase in the Rat Model of Polycystic Ovary Syndrome Induced by Dihydrotestosterone" in Experimental and Clinical Endocrinology and Diabetes, 123, no. 5 (2015):303-307,
https://doi.org/10.1055/s-0035-1548929 . .