| Summary: | Hypertension has a serious harmful effect on the physiological and biochemical functions of heart that end with the appearance of cardio-vascular diseases. Asymmetric dimethylarginine (ADMA) has evolved as an important regulator of nitric oxide (NO) synthesis. The relationship between ADMA and essential hypertension has been scarcely explored. This study is aiming to investigate the physiological, pathological, and biochemical roles of plasma ADMA in relation to serum nitric oxide and also the relation between ADMA and NO with other traditional cardiovascular risk factors in hypertensive patients.
Methods: The study was designed as a prospective case-control study which included 60 hypertensive cardiovascular patients and 10 healthy volunteers as a control group. The patients were divided into four groups: hypertension with cardiovascular complications, uncontrolled hypertension (blood pressure >139/89), controlled hypertension, and control group. Levels of ADMA and nitric oxide were assessed and statistically correlated to other clinical and laboratory values [cholesterol, triglycerides, urea, creatinine, and fasting and postprandial blood sugar].
Results: The plasma ADMA level in group I was significantly increased (2.29 ± 0.06 μmol/L) compared to control group (0.55 ± 0.05 μmol/L) P = 0.001 and also serum NO level was significantly decreased in this group (11.65 ± 0.75 μmol/L) compared to control group (52.11 ± 1.43 μmol/L) P = 0.001. This group had variable complications, e.g., ischemic heart disease, pulmonary hypertension, pulmonary embolism, and cerebrovascular disease. Group II: plasma ADMA level was significantly increased in this group (1.41 ± 0.06) and also serum NO level was significantly decreased (30.91 ± 1.31) compared to control group (P = 0.001). Group III: they had a lower plasma level of ADMA (1.11 ± 0.05) compared to groups I and II (P value: 0.001) and significantly higher than the control group. The serum NO level was significantly decreased (40.01 ± 0.67) compared to control group and significantly higher than groups I and II. Hypertensive groups I, II, and III showed a significant increase in mean fasting and postprandial blood sugar (171.4 ± 71.00, 143.64 ± 37.00, and 137.00 ± 27.06 mg/dl, respectively) compared to control group (85.32 ± 13.17 mg/dl). Urea, creatinine, cholesterol, and triglycerides in the hypertensive groups (I, II, and III) showed a significant increase compared to control group with significant positive correlation in relation to ADMA.
Conclusions: ADMA is elevated in hypertensive patients. Elevated ADMA concentrations are associated with impaired endothelium functions, which are demonstrated by NO reduction in the sera of hypertensive patients. ADMA is correlated positively with the traditional cardiovascular risk factors. Also there was a strong significant negative correlation between NO and ADMA levels in the whole hypertensive groups.
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