Nitric Oxide and Malondialdehyde in Human Hypertension

Abstract

Nitric oxide (NO), a multifunctional effector molecule that plays a central role in the maintenance of vascular homeostasis, regulates vascular tone and inhibits platelet and leukocyte adhesion to endothelial cells. NO status is related to the endothelial function. Patients with hypertension have lower levels of NO, increased free radical production, higher oxidative stress, augmented platelet aggregation, and a change in the arachidonic acid cascade metabolism, all leading to the acceleration of the atherosclerotic process. The study subjects included a group of 21 normotensive healthy subjects (8 males and 13 females) with a mean age of 39.2 +/- 1.8 years and a body mass index of 27.9 kg/m, and another group of 42 patients (19 males and 23 females) with untreated essential hypertension with a mean age of 47.6 +/- 1.7 years and a body mass index of 28.3 kg/m. Serum levels and urinary excretion of NO determined as combined nitrate/nitrite (NOx) and serum malondialdehyde (MDA) concentrations were measured in the 2 groups of subjects. The serum levels and 24-hour urinary excretion of NOx were significantly higher and the renal clearance of NO was lower in the normotensive group than in the hypertensive patients, indicating decreased NO status in hypertension. There was a negative correlation between serum NO levels and mean arterial pressure, suggesting that a decrease in NO availability is related to increase in blood pressure. Serum concentrations of MDA were higher in the hypertensive patients as compared with the normotensive individuals, suggesting increased oxidative stress in hypertensive patients. These results are in agreement with previous studies showing decreased NO and increased oxidative stress in hypertension. In conclusion, patients with essential hypertension as compared with normotensive individuals have lower NO status, which may contribute to the endothelial dysfunction in hypertension. Increased serum malondialdehyde in hypertensives suggests an association between increased oxidative stress with higher blood pressure.

Flax lignan concentrate reverses alterations in blood pressure, left ventricular functions, lipid profile and antioxidant status in DOCA-salt induced renal hypertension in rats

“…Several clinical investigations showed that serum concentrations of MDA are high in the hypertensive patients than in normal individuals. 68 In this study, serum MDA levels were significantly increased, while GSH and SOD levels were significantly decreased in the heart and kidney tissues of the DOCA-salt hypertensive group compared to the UNTZD control group. This indicates that the increase in blood pressure is responsible for the production of oxidative stress.…”

Redox Control of Renal Function and Hypertension

“…NO is another biomolecule with antioxidant functions, and decreased NO is associated with increased oxidative stress and hypertension (3,23,111,118,167). NO bioavailability has been shown to be decreased in advanced atherosclerotic lesions in humans attributed to lower expression of eNOS (361).…”

Endothelial damage in white coat hypertension: role of lectin-like oxidized low-density lipoprotein-1

“…However, the etiology and mechanisms of these relationships, particularly the question of whether impaired NOx precedes or follows HT remain unclear. 28 NOx levels have been reported to be higher, 29 unaffected 30 and lower [31][32][33][34] in various studies. These contradictory results may be due to genetic variations as NOS polymorphism may affect transcription or the function of NOx.…”