The Influence of Hyperthyroidism and Hypothyroidism on the β-Adrenergic Responsiveness of the Turkey Erythrocyte

Bilezikian, John P.; Loeb, Jacques; Gammon, Donald E.

doi:10.1172/jci109288

Cited by 68 publications

(37 citation statements)

References 36 publications

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“…Similar decreases in receptor number have been observed in other tissues (1 The KH and KL of the isoproterenol competition curves were both altered significantly in the hypothyroid cells but the fold change in KH (2.4-fold) was much greater than that in the KL (1.2-fold). There was a concomitant significant decrease in the KLIKH ratio while no significant change was seen in the percent RH (Table I).…”

Section: Resultssupporting

confidence: 78%

“…Thyroid hormone levels appear to modulate tissue responsiveness to beta adrenergic catecholamines, with increased responsiveness often observed in hyper-and decreased responsiveness in hypothyroidism (1,2). Thyroid hormones regulate the number of beta adrenergic receptors in several tissues including rat heart (3), skeletal muscle (4), and submaxillary gland (5) as well as in turkey erythrocytes (1).…”

Section: Introductionmentioning

confidence: 99%

“…Thyroid hormones regulate the number of beta adrenergic receptors in several tissues including rat heart (3), skeletal muscle (4), and submaxillary gland (5) as well as in turkey erythrocytes (1).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hypothyroidism modulates beta adrenergic receptor adenylate cyclase interactions in rat reticulocytes.

Stiles¹,

Stadel²,

Léan³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We have investigated alterations in beta adrenergic receptor binding sites of rat reticulocytes occurring in animals rendered hypothyroid by thyroidectomy. Beta adrenergic receptor interactions were assessed by measuring the number of (-)[3H]-dihydroalprenolol binding sites and the ability of an agonist to compete for occupancy of the receptors. The number of receptors was significantly reduced in cells from the hypothyroid animals. In addition, there were significant agonist-specific alterations in binding. Using computer assisted curve fitting techniques, it was found that the ability of (-)isoproterenol to stabilize a high affinity guanine nucleotide sensitive "coupled" form of the receptor was impaired. Reticulocytes from hypothyroid animals have, in addition, a reduction in the concentration of the nucleotide regulatory protein as assessed by the number of 42,000 Mr substrates for cholera toxin catalyzed ADP ribosylation. These alterations are associated with reductions in catecholamine and NaF stimulated adenylate cyclase activity. Diminished coupling of beta adrenergic receptors with other regulatory components of the adenylate cyclase system represents a mechanism by which altered thyroid states modulate beta adrenergic receptor function and beta adrenergic responsiveness of tissues.

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Section: Resultssupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hypothyroidism modulates beta adrenergic receptor adenylate cyclase interactions in rat reticulocytes.

Stiles¹,

Stadel²,

Léan³

et al. 1981

J. Clin. Invest.

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“…The clinical picture of the thyroid storm is characterized by four main features: (1) Fever 20,21 , (2) sinus tachycardia or a variety of supraventricular arrhythmias (paroxysmalatrial tachycardia, atrial flutter and atrialfibrillation), often accompanied by various degrees of congestive heart failure 17,22 , (3) central nervous system symptoms (agitation, restlessness, confusion, delirium andcoma) [13][14][15][16][17][18][19][20][21][22][23][24][25] , and finally (4) gastrointestinal symptoms, in particular vomiting, diarrhea, intestinal obstruction. 26,27 Unexplained jaundice is suggestive for thyroid storm, but is a poor prognostic sign.…”

Section: Thyrotoxic Crisismentioning

confidence: 99%

Recent Advancement on Current Trend in the Management of Endocrine Emergency in Critically Ill Patient

Ferdous

Afsana

Qureshi

et al. 2016

J. Bangladesh Coll. Phys.

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Summary:Endocrine emergencies represent a group of potentially lifethreatening conditions that are frequently overlooked, resulting in delays in both diagnosis and treatment, factors that further contribute to their already high associated mortality rates. Although endocrine emergencies are often encountered in patients with a known endocrinopathy, the emergency may be the initial presentation in previously undiagnosed individuals. If these endocrine disorders are not rapidly identified or if specific treatment is delayed, significant complications or even death may occur. Careful evaluation of clinical history and a high degree of suspicion are the corner stone to diagnose such problems. Aggressive management of the patient is equally important as the complications are devastating and can prove highly fatal. The present article is an attempt to review some of the common endocrine emergencies in intensive care unit and the challenges associated with their diagnosis and management.

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“…In some (4-13) but not all (13)(14)(15) studies, hyperthyroidism has been associated with an increased number of beta receptors and hypothyroidism with a decreased number of beta receptors. These latter investigations, however, have been limited mainly to a description of the beta receptor itself or the beta receptor-adenylate cyclase complex, and they have not included an examination of possible physiological correlates of changes in beta receptor number (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)15). To this end, it has been desirable to study an experimental tissue that not only possesses a beta-adrenergic receptor but that additionally exhibits a characteristic and readily measurable physiological response to beta-adrenergic agonists in vitro.…”

mentioning

confidence: 99%

Beta-Adrenergic Receptors and Isoproterenol-stimulated Potassium Transport in Erythrocytes from Normal and Hypothyroid Turkeys

Furukawa¹,

Loeb²,

Bilezikian³

1980

J. Clin. Invest.

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A B S T R A C T We have previously reported that in hypothyroid turkeys the number of beta-adrenergic receptors in intact erythrocytes is reduced by -50% without any changes in the affinity of the receptor for the agonist, isoproterenol. In view of the physiological action of the catecholamines to stimulate bidirectional ion fluxes in these cells, we have now examined the possibility that the decrease in beta receptor number might be associated with concomitant changes in catecholamine-dependent potassium ion transport. Hypothyroid turkey erythrocytes display decreased sensitivity to isoproterenol-stimulated potassium influx.Half-maximal stimulation of potassium influx occurs at 9.2±+1.7 nM in hypothyroid cells as opposed to only 3.8±+0.4 nM in normal cells (P < 0.005). A maximal stimulatory concentration of isoproterenol (100 nM) leads to the same increment in ion flux in erythrocytes from hypothyroid and normal turkeys. Analysis of the quantitative relationship between isoproterenol concentration, receptor occupancy, and associated effects upon potassium influx shows that at low levels of isoproterenol, where occupancy is linear with agonist concentration, occupation of a given number of beta receptors leads to a stimulation of potassium transport that is identical in erythrocytes from normal and hypothyroid turkeys. Thus, decreased sensitivity to catecholamine-stimulated potassium transport in hypo-

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The Influence of Hyperthyroidism and Hypothyroidism on the β-Adrenergic Responsiveness of the Turkey Erythrocyte

Cited by 68 publications

References 36 publications

Hypothyroidism modulates beta adrenergic receptor adenylate cyclase interactions in rat reticulocytes.

Hypothyroidism modulates beta adrenergic receptor adenylate cyclase interactions in rat reticulocytes.

Recent Advancement on Current Trend in the Management of Endocrine Emergency in Critically Ill Patient

Beta-Adrenergic Receptors and Isoproterenol-stimulated Potassium Transport in Erythrocytes from Normal and Hypothyroid Turkeys

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