Serum concentration of Apelin and Asymmetric Dimethylarginine in hypertensive patients on different modalities of treatment

Purpose: Hypertension (HTN) is considered a major health problem. Apelin (AP) a novel multifunction peptide implicated in regulation of the cardiovascular system, including blood pressure and cardiac function control, Evidence has accumulated that asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide (NO) synthase. ADMA inhibits vascular NO production at concentrations found in pathophysiological conditions. However, there is no data about ADMA and apelin levels in essential hypertension and any relationship between them and the effect of antihypertensive drugs from various classes on these parameters of endothelial function. The aim of this study is to assess the status of Apelin and Assymetric DiMethyl Arginine in essential Hypertension on various modalities of treatment. Methods: The present study is a cross-sectional study (2007/2008) at Al-Yarmouk Teaching Hospital. Includes measurement of serum AP and ADMA in patients with hypertension. a total of 80 patients with HTN were involved in this study, they were classified according to modality of treatment as Hypertensives on captopril G1: (n=40); Hypertensives on atenolol G2: (n=40). A matching group of eighty apparently healthy volunteers who were included as controls (n=80. Results: Serum AP was significantly reduced and serum ADMA was significantly elevated in hypertensive patients (G1 & G2) as compared with controls (G3) (p < 0.001), also the above significant alteration in these two parameters was found when hypertensives on atenolol (G2) were compared with hypertensives on captopril (G1) (p < 0.001). AP was negatively correlated with ADMA (r = -0.9, p<0.05 for G1) (r = -0.8, p<0.05 for G2); however, this correlation was lost in control group. Conclusion: Patients with HTN have high level of serum ADMA associated with low level of AP compared with controls, both AP and ADMA were negatively correlated; this was most pronounced in G2 indicating positive effects of captopril on NO pathway. [Cukurova Med J 2013; 38(1.000): 1-6]