Table of Contents
ISRN Hypertension
Volume 2013 (2013), Article ID 516528, 5 pages
http://dx.doi.org/10.5402/2013/516528
Research Article

Serum Asymmetric Dimethylarginine Concentrations in Two Models of Experimentally Induced Hypertension

1Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran
2Department of Physiology, Hamadan University of Medical Sciences, Hamadan, Iran
3Department of Immunology, Isfahan University of Medical Sciences, Isfahan, Iran

Received 13 November 2012; Accepted 2 December 2012

Academic Editors: M. Frick, K. Kotani, R. S. Padwal, and G. L. Schwartz

Copyright © 2013 M. Khazaei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The aim of this study was to evaluate the effect of two models of hypertension on serum ADMA concentrations and whether the changes of serum ADMA concentrations are reversible by removing the cause of hypertension. Materials and Methods. 48 male wistar rats were randomly assigned into four groups: control, deoxycorticosterone acetate salt (DOCA-Salt), sham, and two kidneys one clip (2K1C). After 12 weeks, in half of the animals ( each group), serums were taken and direct blood pressure was measured. Then, DOCA injection was withdrawn and the animals received tap water and, in 2K1C group, renal clips were removed. After 12 weeks, direct blood pressure was measured and blood samples were taken. Results. Serum ADMA concentration in DOCA-Salt group was slightly higher than control, although it was not statistically significant. In 2K1C hypertensive group, serum ADMA concentration was significantly elevated compared to sham group ( ). Unclipping and reversal of hypertension returned serum ADMA level to sham group. There was a weak positive correlation between systolic blood pressure and serum ADMA concentration. Conclusion. increased serum ADMA concentration during hypertension is dependent on the model of hypertension, and removing the cause of hypertension could reduce it