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Angiotensin-converting enzyme in human prostate.

M Yokoyama, K Hiwada, T Kokubu

    Clinica Chimica Acta; International Journal of Clinical Chemistry
    |January 31, 1980
    PubMed
    Summary
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    Benign prostatic hyperplasia significantly elevates angiotensin-converting enzyme levels in prostate tissue. This enzyme, found primarily in the soluble fraction, is competitively inhibited by captopril.

    Area of Science:

    • Biochemistry
    • Urology
    • Enzymology

    Background:

    • Angiotensin-converting enzyme (ACE) plays a role in the renin-angiotensin system.
    • ACE activity in the human prostate, particularly in benign prostatic hyperplasia (BPH), is not well characterized.

    Purpose of the Study:

    • To quantify and characterize angiotensin-converting enzyme activity in normal and hyperplastic human prostate tissue.
    • To investigate the kinetic and inhibitory properties of human prostatic ACE.

    Main Methods:

    • Spectrophotometric assay using Hippuryl-L-histidyl-L-leucine (Hip-His-Leu) to measure ACE activity.
    • Partial purification of ACE from benign hypertrophic prostate tissue.
    • Determination of enzyme kinetics, molecular weight, pI, optimal pH, and inhibition by captopril.

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    Main Results:

    • Benign hypertrophic prostate tissue exhibited significantly higher ACE concentration (1.99 units/g) compared to normal prostate tissue (0.44 units/g).
    • Over 80% of ACE activity was found in the soluble fraction of both normal and hypertrophied prostates.
    • Partially purified prostatic ACE showed an apparent molecular weight of 290,000, pI of 4.1, optimal pH of 7.8, and competitive inhibition by captopril (Ki = 1.8 nmol/l).

    Conclusions:

    • Human benign prostatic hyperplasia is associated with significantly increased angiotensin-converting enzyme activity.
    • Prostatic ACE shares characteristics with other known ACE enzymes, including inhibition by captopril.
    • These findings suggest a potential role for ACE in the pathophysiology of benign prostatic hyperplasia.