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Testosterone treatment increases thromboxane function in rat cerebral arteries.

Rayna J Gonzales1, Amir A Ghaffari, Sue P Duckles

  • 1Department of Pharmacology, College of Medicine, Univ. of California, Irvine, CA 92697-4625, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|March 15, 2005
PubMed
Summary

Testosterone treatment increases thromboxane A2 (TxA2) synthase in rat cerebral arteries, enhancing TxA2-mediated vascular tone. This may increase risks for vasospasm and thrombosis in cerebrovascular disease.

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Vascular Biology

Background:

  • Testosterone administration in vivo increases cerebral artery tone.
  • A potential mechanism involves enhanced vasoconstriction via the thromboxane A2 (TxA2) pathway.
  • The role of testosterone in regulating TxA2 synthase and its contribution to cerebrovascular tone requires further investigation.

Purpose of the Study:

  • To investigate the effect of chronic testosterone treatment on TxA2 synthase levels in rat middle cerebral arteries (MCAs).
  • To determine the contribution of TxA2 to vascular tone in testosterone-treated rats.

Main Methods:

  • Immunofluorescence and confocal microscopy to localize TxA2 synthase.
  • Western blot analysis to quantify TxA2 synthase protein levels.

Related Experiment Videos

  • In vitro assessment of vascular responses in pressurized MCA segments.

    • Main Results:

    • TxA2 synthase was detected in both smooth muscle and endothelial layers of MCAs.
    • Testosterone treatment increased TxA2 synthase protein levels in cerebral vessels.
    • Dilation responses to a TxA2 synthase inhibitor and TP antagonist were enhanced in testosterone-treated rats.
    • Endothelium removal abolished the enhanced dilation response to the TxA2 synthase inhibitor, indicating an endothelial mechanism.

    Conclusions:

    • Chronic testosterone treatment enhances TxA2-mediated vascular tone in rat cerebral arteries.
    • This enhancement is primarily due to increased endothelial TxA2 synthesis.
    • Elevated cerebrovascular TxA2 synthase may contribute to the risk of vasospasm and thrombosis in cerebrovascular disease.