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The effect of antihypertensive therapy on abnormal leucocyte sodium transport in essential hypertension

L Poston, R B Jones, P J Richardson

    Clinical and Experimental Hypertension
    |January 1, 1981
    PubMed

    Insights

    Essential hypertension is linked to abnormal sodium transport in white blood cells (leucocytes). This abnormality, characterized by reduced sodium efflux, is corrected by diuretic treatment, suggesting a circulating inhibitor may be involved.

    Area of Science:

    • Cardiovascular Physiology
    • Cellular Biology
    • Renal Physiology

    Background:

    • Essential hypertension is a complex condition with multifactorial origins.
    • Alterations in cellular ion transport have been implicated in the pathophysiology of hypertension.
    • Leucocyte sodium transport offers a potential biomarker for hypertensive disease.

    Purpose of the Study:

    • To investigate sodium transport kinetics in leucocytes of patients with essential hypertension.
    • To determine the effect of diuretic therapy on leucocyte sodium transport.
    • To explore the potential role of circulating factors in modulating sodium transport in hypertension.

    Main Methods:

    • Sodium efflux rate constants were measured in leucocytes from untreated essential hypertensives and normotensive controls.
    • Ouabain-sensitive and insensitive sodium efflux pathways were analyzed.
    • The impact of diuretic treatment on these parameters was assessed.

    Main Results:

    • Untreated essential hypertensives exhibited significantly depressed total and ouabain-sensitive sodium efflux rate constants in leucocytes compared to controls.
    • Diuretic therapy normalized these depressed sodium efflux values.
    • The findings suggest a functional impairment in sodium transport in leucocytes of essential hypertensives.

    Conclusions:

    • A circulating inhibitor of sodium transport may contribute to the pathophysiology of essential hypertension.
    • Leucocyte sodium transport abnormalities are present in essential hypertension and are responsive to diuretic treatment.
    • Further research is warranted to identify the specific circulating inhibitor and its mechanism of action.

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