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Blood viscosity: a pathogenetic factor in the development of essential hypertension?
Insights
Adolescent hypertensives show reduced erythrocyte deformability, impacting blood flow. This occurs independently of Na-K-ATPase function, suggesting altered hemorheology in early hypertension.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Hemodynamics
Background:
- Essential hypertension is linked to sodium transport and blood viscosity.
- Erythrocyte deformability is crucial for hemorheology and is affected by Na-K-ATPase inhibition.
- Understanding these factors in adolescents is key to early hypertension management.
Purpose of the Study:
- To investigate hemorheology and sodium transport in adolescent hypertensives.
- To compare erythrocyte deformability and related parameters with normotensive controls.
- To explore potential links between altered hemorheology and early hypertension.
Main Methods:
- Recruited 73 normotensive and 53 hypertensive adolescents (23-27 yrs).
- Measured blood viscosity, hematocrit, plasma fibrinogen, and erythrocyte deformability using a positive pressure filter system.
- Assessed Na-K-ATPase activity, K+-uptake, and urinary sodium excretion via 86Rb uptake and electrolyte analysis.
Main Results:
- Hypertensives exhibited significantly reduced erythrocyte deformability (Q = 1.77 +/- 0.05) compared to normotensives (Q = 1.64 +/- 0.04).
- No significant differences were found in whole blood viscosity, hematocrit, or plasma fibrinogen.
- Erythrocyte deformability changes were not linked to Na-K-pump inhibition or altered K+-uptake; a slight, non-significant increase in urinary sodium excretion was observed in hypertensives.
Conclusions:
- Adolescent hypertension is associated with decreased erythrocyte deformability, independent of Na-K-ATPase function.
- Altered hemorheology, specifically reduced erythrocyte flexibility, may play a role in early hypertension.
- Further research is needed to clarify the contribution of decreased erythrocyte deformability to increased peripheral vascular resistance in essential hypertension.
Abstract:
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.