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Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney.

Publication ,  Journal Article
Pracyk, JB; Lappi, SE; Slotkin, TA
Published in: J Pharmacol Exp Ther
February 1991

The role of thyroid status in the ontogeny of beta adrenergic receptor control of ornithine decarboxylase (ODC) activity was assessed in hearts and kidneys of neonatal rats. Hyperthyroidism induced by administration of tri-iodothyronine on postnatal days 1 to 5 caused a reduction in the ability of isoproterenol to stimulate cardiac ODC but subsequently accelerated the onset of the postweaning peak of the response; the latter effect was even more prominent when tri-iodothyronine administration was given on postnatal days 14 to 18. Hypothyroidism induced by propylthiouracil administration led to persistent subsensitivity of the cardiac ODC response to beta receptor stimulation. Kidney ODC, which does not become subject to beta receptor regulation until after weaning, was resistant to hyperthyroid-induced changes in reactivity, but hypothyroidism still resulted in long-term response deficits. These results suggest that thyroid hormone is permissive for normal development of the beta receptor-ODC link, and that the euthyroid state provides the optimal conditions for maturation of this signal transduction mechanism. The relative resistance of kidney ODC responses to alterations by hyperthyroidism further indicates that the effects of excess hormone can only be expressed when the receptor-enzyme link is already competent. Finally, thyroid status had equivalent effects on the abilities of vasopressin or angiotensin to stimulate ODC, suggesting that the site of thyroid hormone action is at a transduction locus common to several different receptor types.

Duke Scholars

Published In

J Pharmacol Exp Ther

ISSN

0022-3565

Publication Date

February 1991

Volume

256

Issue

2

Start / End Page

757 / 766

Location

United States

Related Subject Headings

  • Thyroid Hormones
  • Receptors, Adrenergic, beta
  • Rats
  • Propylthiouracil
  • Pregnancy
  • Pharmacology & Pharmacy
  • Ornithine Decarboxylase
  • Myocardium
  • Kidney
  • Hypothyroidism
 

Citation

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Pracyk, J. B., Lappi, S. E., & Slotkin, T. A. (1991). Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney. J Pharmacol Exp Ther, 256(2), 757–766.
Pracyk, J. B., S. E. Lappi, and T. A. Slotkin. “Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney.J Pharmacol Exp Ther 256, no. 2 (February 1991): 757–66.
Pracyk JB, Lappi SE, Slotkin TA. Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney. J Pharmacol Exp Ther. 1991 Feb;256(2):757–66.
Pracyk, J. B., et al. “Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney.J Pharmacol Exp Ther, vol. 256, no. 2, Feb. 1991, pp. 757–66.
Pracyk JB, Lappi SE, Slotkin TA. Role of thyroid hormone in the development of beta adrenergic control of ornithine decarboxylase in rat heart and kidney. J Pharmacol Exp Ther. 1991 Feb;256(2):757–766.

Published In

J Pharmacol Exp Ther

ISSN

0022-3565

Publication Date

February 1991

Volume

256

Issue

2

Start / End Page

757 / 766

Location

United States

Related Subject Headings

  • Thyroid Hormones
  • Receptors, Adrenergic, beta
  • Rats
  • Propylthiouracil
  • Pregnancy
  • Pharmacology & Pharmacy
  • Ornithine Decarboxylase
  • Myocardium
  • Kidney
  • Hypothyroidism