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Multiple forms of human plasma renin substrate.

P Eggena, H Hidaka, J D Barrett

    The Journal of Clinical Investigation
    |August 1, 1978
    PubMed
    Summary
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    This study found that excessive stimulation of plasma renin substrate, caused by steroids or uremia, leads to multiple substrate forms. These altered forms may contribute to hypertension by affecting the renin reaction rate.

    Area of Science:

    • Biochemistry
    • Endocrinology
    • Nephrology

    Background:

    • Plasma renin substrate (PRS) is a key component of the renin-angiotensin system.
    • Understanding PRS heterogeneity is crucial for studying hypertension.
    • Steroid excess and uremia are known to affect PRS levels.

    Purpose of the Study:

    • To investigate heterogeneity of plasma renin substrate in conditions of steroid excess and hypertensive disease.
    • To determine if altered PRS forms correlate with specific hypertensive states.

    Main Methods:

    • Analysis of PRS forms using specific antiserum, electrophoretic mobility, and kinetic rate constants.
    • Comparison of PRS in subjects with normal, suppressed, and stimulated levels.
    • Characterization of PRS in patients with renovascular hypertension.

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    Main Results:

    • Multiple PRS forms were observed during excessive stimulation by estrogens, glucocorticoids, or uremia.
    • These additional PRS forms were absent or in trace quantities with normal or suppressed PRS levels.
    • Differences in kinetic rate constants among PRS forms suggest a role in altered renin reaction rates.
    • A non-angiotensin-generating protein, cross-reactive with PRS antiserum, was found in renovascular hypertension patients.

    Conclusions:

    • Excessive stimulation leads to observable heterogeneity in plasma renin substrate.
    • Altered PRS forms and their kinetic properties may contribute to the pathophysiology of hypertension.
    • A distinct PRS-related protein in renovascular hypertension warrants further investigation.