Key result
Hypertensive rat RBCs display increased fibrinogen-induced aggregation and elevated 110 kD membrane protein.
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The development of hypertension is accompanied by changes in the rheological properties of blood, particularly by increased red blood cell (RBC) aggregation leading to further pathological complications. However, it is not clear whether these changes in aggregation are caused only by increased concentrations of plasma adhesion proteins or if alterations in RBC membranes are also involved. The aim of the present study was to determine if RBC aggregability is altered during hypertension and if these changes correlate with alterations in RBC membrane protein concentrations. Aggregability changes were evaluated by comparing fibrinogen (Fb)-induced aggregation of RBCs from spontaneously hypertensive rats (SHR) with RBCs from age matched normotensive Wistar Kyoto (WKY) rats. ANOVA showed a significant increase in dose-dependent Fb-induced aggregation of RBCs in the SHR group. Analysis of Coomassie-stained gels of RBC membrane proteins using SDS-PAGE showed a significant increase in the amount of a protein at 110 kD in the SHR group. These results show that increased RBC aggregability is accompanied by alterations in RBC membrane protein composition during hypertension development.
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Lominadze et al. (2002) studied Hypertension. Hypertension (Spontaneously hypertensive rat strain) vs. Normotensive Wistar Kyoto (WKY) rats was evaluated on Fibrinogen-induced aggregation of red blood cells and RBC membrane protein concentrations. Red blood cells from spontaneously hypertensive rats exhibited significantly increased fibrinogen-induced aggregability and elevated levels of a 110 kD membrane protein compared to normotensive rats.
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