Thyroid hormone regulation of adrenergic receptors and beta-adrenergic responsiveness in the rat submandibular gland

Medina, Jorge H.; Wolfman, Claudia; Stein, Miguelina Levi de; Tumilasci, Omar R.; Houssay, Alberto B.

doi:10.1016/0024-3205(84)90406-5

Cited by 18 publications

(11 citation statements)

References 17 publications

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“…These experiments examined the effect of increased or decreased exposure to thyroid hormone on three complimentary measures of noradrenergic function: beta-receptor binding, reuptake sites (as reflected by desipramine binding (Langer et al, 1981), and alpha-2 receptor binding. Several investigators have reported increased beta-receptor binding in thyrotoxicosis and decreased beta receptor binding in hypothyroidism, without change in apparent affinity (Medina et al, 1984;Williams et al, 1977;Gross and Lues, 1985). Similar to the data in Table 1, the receptor changes have been found generally in peripheral tissues and not in brain.…”

Section: Discussionsupporting

confidence: 68%

“…Many peripheral manifestations of thyrotoxicosis resemble noradrenergic hyperfunction and are reduced by beta-adrenergic antagonists (Bilezikian and Loeb, 1983). Yet, thyrotoxicosis is associated with increased beta-receptor binding and decreased norepinephrine turnover, while hypothroidism has the opposite properties (Medina et al, 1984;Williams et al, 1977;Gross and Lues, 1985;Bilezikian and Loeb, 1982). Thyrotoxicosis has thus been said to constitute a hyperadrenergic state with diminished norepinephrine synthesis (Gross et al, 1980).…”

Section: Introductionmentioning

confidence: 96%

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Thyroid hormone and norepinephrine: Effects on alpha-2, beta, and reuptake sites in cerebral cortex and heart

Ac¹

1988

J. Neural Transmission

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Thyroid hormone produces metabolic effects similar to those of stimulation of noradrenergic receptors. It has been reported, however, that norepinephrine turnover is reduced during thyrotoxicosis and that beta-noradrenergic receptor number is increased. Metabolic effects of thyroid hormone may therefore reduce noradrenergic activity. We examined effects of thyroid hormone administration or production of hypothyroidism with methimazole on receptors associated with regulation of noradrenergic function. Treatment with thyroid hormone increased beta-receptor binding, increased alpha-2 receptor binding, and decreased desipramine binding, opposite to effects of hypothyroidism produced by methimazole. Heart was more sensitive than brain to these effects. These data are consistent with reduced noradrenergic activity during hyperthyroidism, possibly mediated by an increase in autoreceptor function.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 96%

Thyroid hormone and norepinephrine: Effects on alpha-2, beta, and reuptake sites in cerebral cortex and heart

Ac¹

1988

J. Neural Transmission

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“…Considering that the contractile re sponses to CaCh were not significantly dif ferent either in the pregnant or nonpregnant groups, we can rule out the possibility that the increased sensitivity induced by thyroid dysfunction could be related to altered cal cium mobilization as it was observed in rat thymocytes [ 19], It is possible, however, that the increased responsiveness for acetylcho line and oxytocin observed in preparations obtained from hyperthyroid pregnant rats may be due to qualitative and/or quantita tive alterations of membrane receptors or even in some events which occur beyond the receptor level as described in other tissues [8,10,20]. Thus, enhancement of P-adrenoceptor number with proportional increase in maximal isoprenaline response in several tissues is currently associated with the hy perthyroid state [11,21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Induced Thyroid Dysfunction upon Uterine Responsiveness in Strips from Pregnant and Nonpregnant Rats

Medeiros

Calixto

1989

Pharmacology

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The influence of thyroid dysfunction on rat myometrial responsiveness to oxytocin, acetylcholine, CaCl₂ and BaCl₂ was assessed in uterine strips from pregnant and nonpregnant rats. In preparations obtained from hypothyroid nonpregnant rats, oxytocin and acetylcholine concentration-response curves were significantly displaced to the left, whereas myometrial strips from hyperthyroid nonpregnant rats were only supersensitive to acetylcholine. In relation to the pregnant state, T₃ treatment caused an increased myometrial sensitivity to both oxytocin and acetylcholine. In this condition, concentration-response curves for oxytocin did not differ from nonpregnant control animals, whereas acetylcholine was about 300-fold more potent at the ED₅₀ levels compared with those in nonpregnant animals. Either in pregnant or nonpregnant state, maximal responses and ED₅₀ to BaCl₂ did not differ. In addition, thyroid dysfunction did not modify the pattern of CaCl₂-induced contractions in isolated myometrial strips from pregnant rats. This data extended to the myometrium, previous evidence in the literature indicating that thyroid dysfunction may affect uterine responsiveness to agonists.

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“…Induced hyperthyroidism increases the density of beta-I and alpha1 adrenoceptors in the rat submandibular gland: (Medina et at, 1984;Frumilasci et at, 1982). Betoi adrenergic hypersensitivity is not necessarily incompatible with accumulation of intracellular mucus, since in the chronically reserpinized rat the number of heta adrenroceptors in the submrandibular gland is also increased (Cutler ie at, 1981).…”

Section: Discussionmentioning

confidence: 95%

Effects of Thyroxine and Dexamethasone on Rat Submandibular Glands

Sagulin

Roomans

1989

J Dent Res

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Glucocorticoids and thyroxine are known to have a marked effect on the flow rate and protein composition of rat parotid saliva in hormonally intact animals. In the present study, the effects of a one-week treatment of male rats with dexamethasone and thyroxine were studied by electron microscopy and x-ray micro-analysis, and by measurement of the flow rate and determination of the chemical composition of pilocarpine-induced submandibular saliva. Thyroxine had the most extensive effects on the submandibular gland. The acinar cells were enlarged and filled with mucus; the cellular calcium concentration was significantly increased. The flow rate of the submandibular saliva was significantly reduced compared with that in saline-injected control animals. Thyroxine caused an increase in the concentrations of protein, total calcium, and potassium in the saliva. Dexamethasone had no significant effects on gland ultrastructure or on the elemental composition of the acinar cells; flow rate was not affected, but the concentrations of protein, calcium, and potassium were significantly increased. The effects of dexamethasone and thyroxine on the flow rate and protein composition of pilocarpine-induced rat submandibular saliva differ from those reported earlier for rat parotid saliva after simultaneous stimulation with pilocarpine and isoproterenol.

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Thyroid hormone regulation of adrenergic receptors and beta-adrenergic responsiveness in the rat submandibular gland

Cited by 18 publications

References 17 publications

Thyroid hormone and norepinephrine: Effects on alpha-2, beta, and reuptake sites in cerebral cortex and heart

Thyroid hormone and norepinephrine: Effects on alpha-2, beta, and reuptake sites in cerebral cortex and heart

Effect of Induced Thyroid Dysfunction upon Uterine Responsiveness in Strips from Pregnant and Nonpregnant Rats

Effects of Thyroxine and Dexamethasone on Rat Submandibular Glands

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