Blood Viscosity: A Pathogenetic Factor in the Development of Essential Hypertension?

Inhibition of the ouabain-sensitive Na-K-ATPase by digoxin significantly decreases erythrocyte deformability (5). Since first a decrease in this transport system has been discussed as a pathogenetic factor in the development of essential hypertension and second an increase in blood viscosity, due to an increased hematocrit has been observed in elderly hypertensives, hemorheology and sodium transport systems were examined in adolescent hypertensives and compared with age-matched normotensive controls. 73 normotensives (N; mean blood pressure 127/80 mmHg) and 53 hypertensives (H; mean blood pressure 147/94 mmHg) aged 23-27 yrs were randomly selected from an epidemiological survey, covering 1342 adolescents. While apparent whole blood viscosity at different shear rates, hematocrit, plasma fibrinogen were not significantly different, erythrocyte deformability, measured with a positive pressure filter system (pore phi 5 mu) and expressed as Q = delta P/ery.susp.Hct 10%/delta P/plasma was significantly attenuated with Q = 1.77 +/- 0.05 in H, compared to 1.64 +/- 0.04 in N (p less than 0.05) The decrease in erythrocyte deformability was not accompanied by an inhibition of the Na-K-pump nor of total K+-uptake in erythrocytes, both measured with the 86Rb uptake. There was only a slight increase in Na+-excretion in urine of 184.4 + 12.2 mval in H, compared to 162.0 +/- 10.4 mval in N (n.s.). K-/+-excretion and serum electrolytes did not show any difference. Whether the decrease in erythrocyte deformability may contribute to an increase in peripheral vascular resistance in essential hypertension has to be further clarified.