Clinical & Experimental Cardiology
Open Access
ISSN: 2155-9880
+44 1300 500008
ISSN: 2155-9880
+44 1300 500008
Jianjun, Yu CAO, Chu Chao and Yingxue Yang
First Affiliated Hospital of Xian Jiaotong University, China
Posters & Accepted Abstracts: J Clin Exp Cardiolog
Aims/Objectives: The objectives of this study were to investigate the impact of a high salt diet on the PRMT/ADMA/DDAH (protein arginine methyl transferases; dimethylarginine dimethylaminohydrolase) pathway in Dahl salt-sensitive (DS) rats and SS-13BN consomic (DR) rats and to explore the mechanisms that regulate ADMA metabolism independent of blood pressure reduction. Methods: 8-weeks-old male Dahl Salt-Sensitive (SS) rats and SS-13BN (13BN) rats were randomly divided into five groups: SS normal diet group (NaCl 0.3%, SN group), SS high-salt diet group (NaCl 8%, SH group), high salt diet (8% NaCl) and hydralazine (10 mg/kg/d) intragastric administration (SH + HYD group), 13BN normal diet group (containing NaCl 0.3%, BN group), 13BN high-salt diet group (containing NaCl 8%, BH group). The plasma concentration of ADMA and NOx were determined, mRNA and protein expression of PRMT-1, mRNA expression and activity of DDAH, mRNA and protein expression of eNOS in aortic tissue were detected with RT-qPCR and western blot plasma levels of Nitric Oxide (NO) in DS rats given a high salt diet and subjected to intragastric administration of hydralazine (SH + HYD group) were lower than those given a normal salt diet (SN group). Results: There were significant decreases in expression and activity of Dimethylarginine Dimethylaminohydrolase (DDAH) and endothelial NO Synthase (eNOS) in DS rats given a high diet (SH group) in comparison to the SN group. The activity of DDAH and expression of eNOS in the SH + HYD group decreased more significantly than SN group. The mRNA expression of DDAH-1 and DDAH-2 were lowest in the SH group. Conclusion: It suggest that salt, independent of blood pressure, can affect the PRMT-1/ADMA/DDAH system to a certain degree and lead to endothelial dysfunction in Dahl salt-sensitive rats.
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