%0 Journal Article
%T Serum Asymmetric Dimethylarginine Concentrations in Two Models of Experimentally Induced Hypertension
%A M. Khazaei
%A M. Zarei
%A N. Esmaeil
%J ISRN Hypertension
%D 2013
%R 10.5402/2013/516528
%X 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 Then, DOCA injection was withdrawn and the animals received tap water and, in 2K1C group, renal clips were removed.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 1. Introduction Endothelial dysfunction is a major risk factor for cardiovascular disease which is accompanied with reduced nitric oxide (NO) bioavailability [1]. NO has several vascular protective effects including vasodilation, inhibition of platelet aggregartion, smooth muscle cell proliferation, and leukocyte adhesion [2]. Studies indicated that reduced bioavailability of NO by NO synthase inhibitor or increased NO degradation causes endothelial dysfunction [3]. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase and influence NO production [4]. ADMA is produced by protein arginine methyltransferase enzyme (PRMT) and competes with L-arginine, NO precursor, for all the three isoforms of NO synthase [5]. As an NO synthase inhibitor, ADMA has an important role in vascular homeostasis. There is a correlation between ADMA levels and cardiovascular morbidity and mortality [6, 7]. £żADMA is associated by cardiovascular risk factors such as atherosclerosis, hypertension, and diabetes [8]. Elevated level of ADMA has been demonstrated in hyperlipidemia, diabetes mellitus, and peripheral artery disease [9]; however, there is a controversy on the effect of hypertension on serum ADMA concentration. Some clinical studies reported a relationship between hypertension and high
%U http://www.hindawi.com/journals/isrn.hypertension/2013/516528/