Mechanisms of altered beta-adrenergic responsiveness in the hyperthyroid and hypothyroid turkey erythrocyte

Bilezikian, John P.; Loeb, Jacques

doi:10.1016/0024-3205(82)90282-x

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…These data suggest that the increase in beta-adrenergic activity might arise from a direct thyroid hormonemediated increase in adrenergic receptor number via the process of 'upregulation'. Other reports found no change in the beta-adrenergic receptor number in experimental hyperthyroidism (117,124). In animals, beta-adrenergic blockade with propranolol has been shown to reverse the T 3 -mediated drop in SVR (17) and to blunt the increase in cardiac output.…”

Section: The Sympathetic Function In Thyroid Disordersmentioning

confidence: 99%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper-and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the renin-angiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

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Section: The Sympathetic Function In Thyroid Disordersmentioning

confidence: 99%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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“…7 – 13) Futhermore, the number of beta-adrenergic receptors is decreased in the heart of hypothyroid rats 8 , 12) and red blood cells of turkeys. 25) But the application of direct binding studies using a biologically active radiolabeled compound to the investigation of possible molecular alterations of hormone receptors in human disease has been limited by the relative inaccessability of large quantities of human tissue for binding studies.…”

Section: Discussionmentioning

confidence: 99%

Studies on Changes of β-Adrenergic Receptors in Polymorphonuclear Cell and Mononuclear Cell with the Changes of Thyroid Function

Lee

You

Kim

et al. 1986

Korean J Intern Med

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Although it has been well established that thyroid hormones increase β-adrenergic receptors of various tissues in the animal studies, there are controversies about the β-adrenergic receptor changes of human mononuclear cells and polymorphonuclear cells.The present study was performed to analyze the change of β-adrenergic receptor of those cells according to the thyroid functional status and to evaluate their usefulness in assessment of sympathetic hyperactivity. We measured [3H]-dihydroalprenolol binding to circulating mononuclear and polymorphonuclear cells from 18 patients with hyperthyrodism, 7 with hypothyroidism, 8 with euthyroid goiter and 21 normal controls.Only with polymorphonuclear cells the receptor concentration was significantly higher (P<0.01) in hyperthyroidism (46.07±4.78 fmol/mg protein) than in the normal control (28.42±2.06 fmol/mg protein) and the affinity constants of both cells were comparable to normal control values. And serum concentrations of T3 were not correlated well with the changes of receptor concentrations in hyperthyroidism. The patients with hypothyroidism and euthyroid goiter showed no significant difference in the receptor concentration and the affinity constants with both cell binding assays.These results indicate that thyroid hormones increase the receptor concentration in polymorphonuclear cells which might be responsible for the symptoms of sympathetic hyperactivity and the polymorphornuclear cells are useful for β-adrenergic receptor assay.

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“…The receptors for a-and /?-adrenergic stimulation are modulated in states of both hypo-and hyperthyroidism (177,178). In animals, hypothyroid¬ ism gives rise to increased G¡a-and G/3-subunits in adipose tissue, while Gsa levels were normal (179,180).…”

Section: Mutations In Gsa and Gi2amentioning

confidence: 99%

G-Proteins: implications for pathophysiology and disease

Gordeladze

Johansen²,

Paulssen³

et al. 1994

European Journal of Endocrinology

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This article focuses on the involvement of G-proteins in neuroendocrine secretion, cell growth and phenotype alterations. The current concept of hormonal activation of the GTPase cycle, as well as the molecular diversity of G-proteins families and receptor*G-protein*effector coupling, are described. Also described are certain G-proteins as possible proto-oncogenes and how point mutations and frame shift mutations alter G-protein function and determine the characteristics of various endocrine diseases. The article outlines in detail how receptors and G-proteins interact in prolactin and growth-hormone-secreting pituicytes, how G-proteins are involved in the growth and differentiation of preadipocytes and osteoblasts. All in all, it seems that hormonal activation through G-proteins is modulated through direct intra- and inter-signalling system cross-talk at the plasma membrane level (short-term) and through interactions on the level of transcription (HREs) from tyrosine kinases, steroid-like hormones and metabolic pathways. Pharmacological intervention to treat diseases where G-proteins are involved should take both long and short-term regulatory phenomena into consideration.

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Mechanisms of altered beta-adrenergic responsiveness in the hyperthyroid and hypothyroid turkey erythrocyte

Cited by 8 publications

References 32 publications

Vascular and renal function in experimental thyroid disorders

Vascular and renal function in experimental thyroid disorders

Studies on Changes of β-Adrenergic Receptors in Polymorphonuclear Cell and Mononuclear Cell with the Changes of Thyroid Function

G-Proteins: implications for pathophysiology and disease

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