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Phenylephrine induced aortic vasoconstriction is attenuated in hyperthyroid rats.

C I Pantos1, V Tzilalis, S Giannakakis

  • 1Department of Pharmacology, University of Athens, Athens, Greece.

International Angiology : a Journal of the International Union of Angiology
|September 5, 2001
PubMed
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Thyroxine-induced hyperthyroidism in rats shows reduced vascular tension to phenylephrine (PE) in the thoracic aorta. This study investigated vascular responses in a rat model of thyroxine-induced cardiac hypertrophy.

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Vascular Biology

Background:

  • Abnormal vascular responsiveness to vasoconstrictors is implicated in hyperthyroidism's impact on peripheral vascular resistance.
  • Thyroid hormones can influence vascular tone and cardiac function.

Purpose of the Study:

  • To investigate the vascular response to potassium chloride (KCl) and phenylephrine (PE) in a rat model of thyroxine-induced cardiac hypertrophy.
  • To assess if thyroxine treatment alters aortic ring tension and relaxation responses.

Main Methods:

  • Wistar rats were treated with L-thyroxine (THYR) or saline (NORM) for two weeks to induce cardiac hypertrophy.
  • Thoracic aorta rings were isolated and subjected to KCl and PE to measure maximal tension (Tmax) with and without endothelium (+E, -E).

Related Experiment Videos

  • Relaxation response to acetylcholine was assessed as a percentage of PE-induced maximal tension.

    • Main Results:

    • Thyroxine-treated rats exhibited significantly increased left ventricular weight compared to controls.
    • Maximal tension in response to KCl was similar between groups.
    • Maximal tension in response to PE was significantly lower in thyroxine-treated rats, both with and without endothelium.
    • Acetylcholine-induced relaxation was not significantly different between groups.

    Conclusions:

    • Thoracic aorta vascular tension in response to phenylephrine is reduced in thyroxine-treated rats.
    • This reduced tension may be attributed to enhanced phenylephrine-induced vasorelaxation at higher concentrations.
    • The relaxation response to acetylcholine remains unaffected by thyroxine treatment in this model.