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Related Experiment Videos

Renin-angiotensin system in thyroid dysfunction in rats

C Marchant1, L Brown, C Sernia

  • 1Department of Physiology and Pharmacology, University of Queensland, Australia.

Journal of Cardiovascular Pharmacology
|September 1, 1993
PubMed
Summary
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Thyroid dysfunction significantly alters the renin-angiotensin system (RAS) and angiotensin II (AT) receptors, particularly AT2 subtypes. These changes suggest potential therapeutic targets for cardiovascular disease in thyroid disorders.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Thyroid dysfunction profoundly impacts cardiovascular function.
  • The renin-angiotensin system (RAS) plays a critical role in cardiovascular regulation.
  • Understanding the interplay between thyroid hormones and the RAS is crucial for managing cardiovascular complications.

Purpose of the Study:

  • To investigate the effects of experimental hyperthyroidism and hypothyroidism on the plasma RAS and angiotensin II (AT) receptors in rats.
  • To characterize changes in AT receptor subtypes (AT1 and AT2) in cardiac and other tissues under different thyroid states.
  • To explore potential therapeutic implications of these findings for cardiovascular disease associated with thyroid dysfunction.

Main Methods:

Related Experiment Videos

  • Induction of hyperthyroidism and hypothyroidism in rats using triiodothyronine (T3) treatment or propylthiouracil.
  • Measurement of plasma components including angiotensinogen, plasma renin activity (PRA), plasma renin concentration (PRC), and plasma angiotensin II (AT).
  • Quantification of AT receptor densities and subtypes (AT1, AT2) in heart, liver, adrenal gland, and kidney tissues using radioligand binding assays and selective antagonists.

    • Main Results:

    • Hyperthyroidism activated the plasma RAS, increasing angiotensinogen, PRA, and plasma AT. Hypothyroidism suppressed these components.
    • Plasma aldosterone levels were reduced in both hyperthyroid and hypothyroid states.
    • AT receptor densities varied by tissue and thyroid state; cardiac, liver, and kidney AT receptors increased with hyperthyroidism, while adrenal receptors decreased. Hypothyroidism showed similar trends, with a marked increase in adrenal AT receptors.
    • Ventricular AT2-subtype density significantly increased in hyperthyroidism and hypothyroidism, whereas AT1-subtype density decreased in hyperthyroidism.

    Conclusions:

    • Thyroid dysfunction induces significant alterations in the plasma RAS and AT receptor expression, particularly affecting AT2 receptor density.
    • The observed changes in the RAS and AT receptors suggest a complex interaction between thyroid hormones and the cardiovascular system.
    • Targeting AT2 receptors, possibly with selective antagonists, may offer a novel therapeutic strategy for cardiovascular complications in patients with thyroid dysfunction.