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Related Experiment Videos

Endothelial dysfunction in growth hormone transgenic mice.

Irene J Andersson1, Maria E Johansson, Anna Wickman

  • 1Department of Physiology, Institute of Physiology and Pharmacology, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.

Clinical Science (London, England : 1979)
|September 28, 2005
PubMed
Summary

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Excess growth hormone (GH) impairs blood vessel function in a time- and vessel-specific manner, initially due to oxidative stress. This study models cardiovascular disease in acromegaly using bovine GH transgenic mice.

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Molecular Biology

Background:

  • Acromegaly, characterized by growth hormone (GH) overproduction, is linked to cardiovascular disease.
  • Bovine GH (bGH) transgenic mice exhibit hypertension and hypercholesterolemia, serving as a model for acromegaly-related cardiovascular complications.

Purpose of the Study:

  • To investigate the impact of excess GH on vascular endothelial function in bGH transgenic mice.
  • To determine the role of oxidative stress in mediating endothelial dysfunction in this model.

Main Methods:

  • Assessed acetylcholine-induced relaxation in aortic and carotid artery rings from young and aged bGH transgenic and control mice.
  • Evaluated the effect of a free radical scavenger (MnTBAP) on vascular function.
  • Measured mRNA levels of endothelial nitric oxide synthase (eNOS) and extracellular superoxide dismutase (EC-SOD).

Related Experiment Videos

  • Quantified intracellular superoxide anion production in vascular tissue.

    • Main Results:

    • Carotid arteries showed impaired relaxation in bGH mice, while aortic function was affected only in aged mice.
    • MnTBAP partially corrected endothelial dysfunction in young carotid arteries and aged aortas.
    • No difference in superoxide production was observed, but EC-SOD and eNOS mRNA levels increased in young bGH mouse aortas.

    Conclusions:

    • Overexpression of bGH leads to time- and vessel-specific endothelial dysfunction.
    • Oxidative stress is an initial contributor, with other factors becoming involved over time.
    • This model provides insights into vascular alterations in acromegaly.