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Related Experiment Videos

Abnormal prorenin processing in growth hormone deficiency.

Michael S Gordon1, Anne L Caston-Balderrama, Murray B Gordon

  • 1Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. msgordon@bics.bwh.harvard.edu

Growth Hormone & IGF Research : Official Journal of the Growth Hormone Research Society and the International IGF Research Society
|June 22, 2005
PubMed
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Growth hormone deficiency (GHD) is linked to higher cardiovascular mortality due to abnormal prorenin processing and cardiac autonomic dysfunction. Growth hormone (GH) treatment showed a trend toward normalizing these defects.

Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Metabolic Disorders

Background:

  • Growth hormone deficiency (GHD) is associated with increased premature cardiovascular mortality.
  • Cardiac autonomic dysfunction, a risk factor for cardiovascular mortality, is observed in GHD patients.
  • Abnormal prorenin processing, indicated by a reduced renin/prorenin ratio, is linked to cardiac autonomic dysfunction in diabetic patients.

Purpose of the Study:

  • To investigate renin/prorenin ratios in untreated GHD patients, GH-treated GHD patients, and normal controls.
  • To explore the relationship between GHD, prorenin processing, and cardiac autonomic dysfunction.
  • To assess the effect of GH treatment on renin/prorenin ratios.

Main Methods:

  • Comparative study involving three groups: untreated GHD (n=31), GH-treated GHD (n=23), and normal controls (n=59).

Related Experiment Videos

  • Measurement of renin/prorenin ratios in all study groups.
  • Analysis of mean renin/prorenin ratios and statistical comparisons between groups.

    • Main Results:

    • Significantly lower mean renin/prorenin ratios were found in both untreated (0.0765±0.0089) and treated (0.113±0.018) GHD groups compared to normal controls (0.304±0.029) (P<0.01).
    • No significant difference in renin/prorenin ratios was observed between untreated and treated GHD groups (P=NS).
    • GH treatment for a mean duration of 49.4±6.7 months showed a non-significant trend toward normalizing the renin/prorenin ratio.

    Conclusions:

    • GHD is characterized by abnormal prorenin processing, suggesting a link to cardiac autonomic adrenergic dysfunction.
    • This abnormal processing is a potential contributor to the increased cardiovascular mortality risk in GHD.
    • GH treatment may have a beneficial effect on prorenin processing, warranting further investigation.