Abstract
Background: This study investigates the plasma activity of inflammatory mediators such as granulocyte-macrophage colony-stimulating factor (GM-CSF), C-C chemokines and soluble adhesion molecules, produced by monocyte–endothelial cell adhesive interaction, in patients with arterial hypertension. Methods: We studied 66 untreated patients with mild to moderate arterial hypertension (hypercholesterolemic: 34, normocholesterolemic: 32) and 30 sex- and age-matched normocholesterolemic normotensive controls. Plasma concentrations of GM-CSF, macrophage chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), RANTES (regulated on activation normally T-cell expressed and secreted), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), as well as plasma endothelin-1 (ET-1), were determined in study population by ELISA and RIA, respectively. Results: Hypertensives exhibited significantly higher levels of GM-CSF (6.5±1.3 vs. 2.3±0.7 pg/ml, P=0.099), MCP-1 (175±31 vs. 120±24 pg/ml, P=0.0093), MIP-1α (23±4 vs. 15±2 pg/ml, P=0.0089), RANTES (17±4 vs. 14±3 ng/ml, P=0.047), sICAM-1 (235±39 vs. 187±21 ng/ml, P=0.0041), sVCAM-1 (684±42 vs. 589±23 ng/ml, P=0.0045) and ET-1 (6.1±1.5 vs. 2.4±0.3 pg/ml, P=0.0095) than those of normotensives. The normocholesterolemic hypertensives had significantly lower levels of GM-CSF, MCP-1, MIP-1α, sICAM-1 and sVCAM-1 than hypercholesterolemic hypertensives but higher than normotensives. In hypertensives, ET-1 levels were significantly correlated with mean arterial pressure ( r=0.51, P=0.028), MCP-1 values ( r=0.45, P=0.047) and sICAM-1 levels ( r=0.64, P=0.0090). Significant correlations were also found between LDL cholesterol values and plasma inflammatory factors GM-CSF ( r=0.58, P=0.0088), MCP-1 ( r=0.49, P=0.040) and sICAM-1 ( r=0.53, P=0.034) in the hypercholesterolemic sub-group of hypertensives. Conclusions: Inflammatory markers of monocyte–endothelial cell adhesive interaction are elevated in hypertensives in comparison to normotensives and may be related to plasma ET-1 activity. The coexistence of hypercholesterolemia may enhance this inflammatory process induced by arterial hypertension.
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