Relationship between (Na + K)-ATPase activity, lipid peroxidation and fatty acid profile in erythrocytes of hypertensive and normotensive subjects

Abstract

Oxidative stress may play a role in the pathogenic mechanism of essential hypertension. Lipid peroxidation can alter the cellular structure of membrane-bound enzymes by changing the membrane phospholipids fatty acids composition. We investigated the relationship between (Na + K)-ATPase activity, lipid peroxidation, and erythrocyte fatty acid composition in essential hypertension. The study included 40 essential hypertensive and 49 healthy normotensive men (ages 35-60 years). Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking, and any current medication. Patients underwent 24-h ambulatory blood pressure monitoring and blood sampling. Lipid peroxidation was measured in the plasma and erythrocytes as 8-isoprostane or malondialdehyde (MDA), respectively. Antioxidant capacity was measured as ferric reducing ability of plasma (FRAP) in the plasma and as reduced/oxidized glutathione (GSH/GSSG ratio) in erythrocytes. (Na + K)-ATPase activity and fatty acids were determined in erythrocyte membranes. Hypertensives had higher levels of plasma 8-isoprostane, erythrocyte MDA, and relative percentage of saturated membrane fatty acids, but lower plasma FRAP levels, erythrocyte GSH/GSSG ratio, (Na + K)-ATPase activity and relative percentage of unsaturated membrane fatty acids, compared with normotensives. Day-time systolic and diastolic blood pressures correlated positively with lipid peroxidation parameters, but negatively with (Na + K)-ATPase activity. These findings suggest that the modulation of (Na + K)-ATPase activity may be associated with changes in the fatty acid composition induced by oxidative stress and provide evidence of a role for this enzyme in the pathophysiology of essential hypertension.

Impact of Manganese on and Transfer across Blood-Brain and Blood-Cerebrospinal Fluid Barrier in Vitro

“…In the CP epithelium, the Na ϩ ,K ϩ -ATPase is the driving force of the active fluid secretion and is furthermore a major player of various active transport properties including transport of phenol red from apical to basolateral compartment. Disturbance of Na ϩ ,K ϩ -ATPase function might result from an inhibition of the Na ϩ ,K ϩ -ATPase activity, which has been described in neuroblastoma cells or liver tissue by Mn before (45,46), but might also be due ϩ -ATPase has also been reported to be inhibited by ROS in primary cultures (47), and it is generally known that Mn overexposure induces a transient increase in the cellular ROS level of brain cells (48,49). Additionally, chronic Mn exposure might alter systematic homeostasis of calcium, leading to a further impairment of Na ϩ ,K ϩ -ATPase function (14,50).…”

Stabilization of membrane bound ATPases and lipid peroxidation by carotenoids from Chlorococcum humicola in Benzo(a)pyrene induced toxicity

“…However, in this study with mice, higher Na + K + -ATPase activity in the erythrocyte membrane of carcinogen treated mice was observed compared with the control. Carcinogenic effect results depolarization of the membrane at a higher rate than before, efflux of Na + ion will be less in the cancerous condition relative to the normal mice [31] .…”

Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases

“…1; Beltowski et al 2004). Impaired Na C /K C -ATPase function has also been observed in diabetes, hypertension, dyslipidemia, and metabolic syndrome (Koter et al 2004, Chibalin 2007, Rodrigo et al 2007, Javorkova et al 2010. Interestingly, both metformin and statins have been reported to enhance the Na C /K C -ATPase activity of erythrocytes in diabetic and dyslipidemic patients respectively (Chakraborty et al 2011, Uydu et al 2012.…”