Noradrenergic and dopaminergic modulation of thyrotropin secretion in the rat

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dc.contributor.authorJaffer A.
dc.contributor.authorRussell V.A.
dc.contributor.authorTaljaard J.J.F.
dc.date.accessioned2011-05-15T16:15:44Z
dc.date.available2011-05-15T16:15:44Z
dc.date.issued1987
dc.description.abstractNoradrenergic and dopaminergic regulation of thyrotropin (TSH) secretion was investigated in adult male Wistar rats. TSH secretion displayed a circadian variation with peak serum TSH levels at 10.00 h. The α2-adrenoceptor agonist, clonidine (250 μg/kg, i.p.), was found to cause an enhancement of serum TSH levels at 10.00 h (160 ± 10% of control values, P < 0.001) which was antagonized by prior administration of the α2-adrenoceptor antagonist, yohimbine (3 mg/kg, i.p.). The α-adrenoceptor antagonist phentolamine caused a significant decrease in serum TSH levels at 10.00 h (62 ± 15% of control values, P < 0.05) at a dosage of 2 mg/kg, i.p. The α1-adrenoceptor agonist, phenylephrine (0.2 or 2 mg/kg, i.p.), was without effect as were the dopaminergic receptor agonist, apomorphine (1 or 5 mg/kg, i.p.), and the antagonist, sulpiride (20 mg/kg, i.p.). The β-adrenoceptor agonist, isoproterenol (1 mg/kg, i.p.) was found to cause a decrease in serum TSH levels at 10.00 h (70 ± 16% of control levels, P < 0.01), which was completely antagonized by prior administration of the β-adrenoceptor antagonist, propranolol (10 mg/kg, i.p.).TSH-releasing hormone (TRH, 5 μg/kg, i.v.) caused a significant stimulation of TSH secretion (470 ± 63% of basal levels, P < 0.001), which was not affected by prior treatment of the rats with yohimbine (0.1 mg/kg, i.p.), phentolamine (2 mg/kg, i.p.), propranolol (10 mg/kg, i.p.) or sulpiride (20 mg/kg, i.p.). There was, however, a tendency towards a decrease in the TRH-stimulated release of TSH in rats pretreated with phentolamine or propranolol. The results of this study clearly demonstrate the existence of stimulatory α2-adrenoceptors as well as inhibitory β-adrenoceptors which modulate TSH secretion in vivo and which can be used to test noradrenergic receptor responsiveness under different pharmacological conditions.
dc.description.versionArticle
dc.identifier.citationBrain Research
dc.identifier.citation404
dc.identifier.citation1-2
dc.identifier.issn00068993
dc.identifier.urihttp://hdl.handle.net/10019.1/13468
dc.subjectclonidine
dc.subjectisoprenaline
dc.subjectphentolamine
dc.subjectphenylephrine
dc.subjectpropranolol
dc.subjectprotirelin
dc.subjectsulpiride
dc.subjectthyrotropin
dc.subjectyohimbine
dc.subjectanimal experiment
dc.subjectdose time effect relation
dc.subjectdrug antagonism
dc.subjectdrug comparison
dc.subjectdrug efficacy
dc.subjectendocrine system
dc.subjectetiology
dc.subjectintraperitoneal drug administration
dc.subjectnonhuman
dc.subjectpharmacokinetics
dc.subjectpriority journal
dc.subjectrat
dc.subjectAnimal
dc.subjectApomorphine
dc.subjectCircadian Rhythm
dc.subjectDopamine
dc.subjectMale
dc.subjectNorepinephrine
dc.subjectProtirelin
dc.subjectRats
dc.subjectSulpiride
dc.subjectSupport, Non-U.S. Gov't
dc.subjectSympathomimetics
dc.subjectThyrotropin
dc.titleNoradrenergic and dopaminergic modulation of thyrotropin secretion in the rat
dc.typeArticle
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