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Related Experiment Videos

Elevated 18-hydroxy-corticosterone in inbred salt-sensitive rats.

G T Griffing1, J C Melby, M Holbrook

  • 1Evans Memorial Department of Clinical Research, Boston University Medical Center, Massachusetts 02118.

Clinical and Experimental Hypertension. Part A, Theory and Practice
|January 1, 1991
PubMed
Summary

Salt-sensitive rats exhibit elevated steroid hormones like 18-hydroxydeoxycorticosterone (18-OH-DOC) and 19-nor-deoxycorticosterone (19-nor-DOC), linked to adrenal 11 beta-hydroxylase activity. These findings offer insights into hypertension mechanisms.

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Area of Science:

  • Endocrinology
  • Mineralocorticoid Metabolism
  • Hypertension Research

Background:

  • Salt-sensitive hypertension is linked to elevated deoxycorticosterone (DOC) metabolites.
  • The role of adrenal 11 beta-hydroxylase in producing these metabolites in salt-sensitive rats is not fully understood.

Purpose of the Study:

  • To compare urinary steroid products of adrenal 11 beta-hydroxylase in salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats.
  • To investigate the relationship between specific steroid metabolites and hypertension susceptibility.

Main Methods:

  • Measurement of urinary free levels of 18-hydroxydeoxycorticosterone (18-OH-DOC), 19-nor-deoxycorticosterone (19-nor-DOC), corticosterone (B), and 18-hydroxycorticosterone (18-OH-B).
  • Analysis was performed on male and female SS/Jr and SR/Jr rats at 7 and 12 weeks of age on a low-salt diet.

Related Experiment Videos

  • Statistical analysis of steroid levels and their correlations.

    • Main Results:

    • SS/Jr rats showed elevated urinary levels of 18-OH-DOC, 19-nor-DOC, and 18-OH-B compared to SR/Jr rats.
    • Corticosterone (B) levels did not differ between groups.
    • The most significant increase was observed in 18-OH-B, which correlated with 18-OH-DOC and B.

    Conclusions:

    • Salt-sensitive rats exhibit altered adrenal steroidogenesis, with elevated 18-OH-DOC, 19-nor-DOC, and 18-OH-B.
    • These findings suggest a potential role for abnormal adrenal 11 beta-hydroxylase activity in the development of salt-sensitive hypertension.
    • The strong correlation between these steroids indicates a shared biosynthetic pathway influenced by adrenal 11 beta-hydroxylase.