Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A subcutaneous injection of an oil suspension of l-epinephrine (270 mumol/kg), dopamine (270 mumol/kg) or l-norepinephrine (270 mumol/kg), when administered with phenoxybenzamine (32 mumol/kg i.p.) to blocl alpha adrenergic effects, increases the cyclic 3', 5'-adenosine monophosphate (cAMP) content in superior cervical ganglia (SCG) of rats. The increase is highest after l-epinephrine and dopamine and is barely detectable after l-norepinephrine; it lasts longer than 2 hours after l-epinephrine, about 30 minutes after dopamine and is fleeting after l-norepinephrine. The duration of the increase in cAMP elicited by l-epinephrine in SCG of rats is dose-related. Furthermore, when the cAMP increase lasts longer than 90 minutes, 48 hours later the tyrosine hydroxylase (TH) activity in SCG is increased. l0Epinephrine (150 mol/kg s.c.) induces TH in decentralized ganglia. One injection of l-isoproterenol (77 mol/kg i.p.) increases cAMP concentrations in intact and decentralized SCG. This increase lasts only 30 minutes and fails to induce TH 48 hours later. However, if the increase of cAMP concentration is prolonged by four successive injections of l-isoproterenol (15 30-minute intervals) the TH activity of intact and decentralized SCG is increased 48 hours later.l-Isoproterenol (four injections of 77 mumol/kg, each) and l-epinephrine (270 mumol/kg) fail to induce TH in the adrenal medulla. dl-Propranolol (125 mumol/kg i.p.) injected 30 minutes before l-isoproterenol blocks the increase of cAMP content and the delayed induction of TH activity in SCG. The elevation of TH activity elicited in SCG by beta adrenergic receptor agonists is always preceded by an increase of cAMP concentration lasting 90 minutes or longer. However, the induction of TH elicited by cold exposure or by reserpine administration can occur without an apparent increase in ganglionic cAMP concentration.
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PMID:Induction of tyrosine hydroxylase elicited by beta adrenergic receptor agonists in normal and decentralized sympathetic ganglia: role of cyclic 3',5' - adenosine monophosphate. 23 17

A 21-year-old goitrous hypothyroid Chinese woman had elevated serum iodotyrosines with a monoiodotyrosine level of 85.9 nmol/l (normal 0.49-0.89 nmol/l) and a diiodotyrosine level of 25.3 nmol/l (normal 0.023-0.53 nmol/l). She was amenorrheic with low luteinizing hormone and follicle-stimulating hormone levels at 5.8 and 2.8 U/l, respectively. The hypogonadotropic hypogonadism was due to an elevated prolactin level of 8.8 nmol/l. She also had a low potassium level of 3.2 mmol/l, and a high urinary aldosterone level of 158 nmol/day. The hyperprolactinemia, hypogonadotropic hypogonadism, hyperaldosteronism and hypokalemia subsided with the administration of bromocriptine 5 mg/day. However, bromocriptine accentuated the hyperiodotyrosinemia, and the patient remained hypothyroid. Levothyroxine therapy lowered the monoiodotyrosine and diiodotyrosine levels, ameliorated all her endocrinopathies, started her periods, and shrank the goiter. She probably had a deiodinase defect which permitted the discharge of accumulated iodotyrosines from the thyroid gland. Since iodotyrosines are tyrosine hydroxylase inhibitors, the hyperiodotyrosinemia causes dopamine synthesis inhibition, and induces the hyperprolactinemia and hyperaldosteronism.
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PMID:Hyperiodotyrosinemia-induced hyperprolactinemia and hyperaldosteronism. 212 37

Intracellular recordings were made from neurons of vesical parasympathetic ganglia (VPG) isolated from the rabbit urinary bladder and maintained, in vitro. Bath-application of norepinephrine (NE, 500 nM-5 microM) caused a hyperpolarizing response at the postsynaptic membrane of VPG neurons in a concentration-dependent manner. NE blocked the action potential elicited by an orthodromic stimulation of preganglionic (pelvic) nerve fibers. At a relatively low concentration (5-100 nM), NE depressed the fast excitatory postsynaptic potential (EPSP), without producing the hyperpolarization. NE (100 nM) produced 49 +/- 17% (N = 5) decrease in the amplitude of the fast EPSP. NE did not depress the acetylcholine (ACh) potential produced by iontophoretic application of ACh to the ganglion cells. NE did not affect the amplitude of the miniature EPSP, while it reduced the frequency of miniature EPSPs. These results suggest that NE inhibits the nicotinic transmission in the rabbit VPG, probably reducing the ACh release from presynaptic nerve terminals. Epinephrine (1 microM) was more potent than NE (1 microM) in producing the hyperpolarization as well as the blockade of the fast EPSP amplitude. Isoproterenol was ineffective as an agonist for these inhibitory adrenoceptors. Clonidine mimicked the effect of NE on the fast EPSP. Yohimbine and idazoxan antagonized both the inhibition of the fast EPSP and the hyperpolarization produced by NE. These results suggest that alpha 2-adrenoceptors are responsible for the inhibition of the neuronal activity in parasympathetic ganglia of the rabbit urinary bladder. Immunohistochemical study demonstrated the presence of tyrosine hydroxylase (TH)-labelled neuronal elements in the VPG. They were a small proportion of principal neurons, their dendrites, and many varicose fibers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha 2-adrenoceptors mediate the inhibition of cholinergic transmission in parasympathetic ganglia of the rabbit urinary bladder. 216 Jul 41

The involvement of adrenal hormones as regulatory factors in maintaining physiological levels of tyrosine hydroxylase (TH) was examined in mouse superior cervical ganglion. Following bilateral adrenalectomy, TH activity in the ganglion fell at a slow but steady rate, reaching 60-65% of the control levels after 2 weeks. Decentralization is known also to reduce TH activity in the ganglion. The effects of adrenalectomy and decentralization were therefore compared, and they were found to be additive, indicating different mechanisms in the two cases. The reduction of TH activity following adrenalectomy was not prevented by replacement with corticosterone (0.5 mg/kg, daily). However, replacement with epinephrine (4 mg/kg, daily) completely prevented the fall of TH activity in adrenalectomized animals. Isoproterenol, a beta-adrenergic receptor agonist, was as effective as epinephrine in preventing the reduction of TH activity following adrenalectomy. Furthermore, in intact animals, chronic administration of SKF 64139, an inhibitor of adrenal PNMT which depletes circulating epinephrine levels, also reduced ganglionic TH activity to the same level as that after adrenalectomy. These results indicate that epinephrine, but not corticosterone, is the adrenal factor required for physiological maintenance of normal levels of TH in the superior cervical ganglion.
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PMID:Adrenal influence on tyrosine hydroxylase activity in superior cervical ganglion. 610 52

The role of the presynaptic alpha and beta-adrenoceptors on the regulation of tyrosine hydroxylase activity was studied in guinea pig atria depolarized with 50 mM K+. The presence of the beta-blocker propranolol (0.1 microM), alpha-blockers phentolamine (0.31 microM) or yohimbine (0.3 microM) or the alpha-agonist clonidine (0.1 microM) in the incubation medium did not affect tyrosine hydroxylase activation by 50 mM K+. On the contrary, the beta-agonist isoproterenol (0.012 microM) potentiated the activation produced by 50 mM K+, effect blocked by propranolol. Also the phosphodiesterase inhibitor, 1-methyl-3-isobutyl-xanthine (100 microM), facilitated tyrosine hydroxylase activation by potassium. Isoproterenol might exert its facilitatory effect through the stimulation of presynaptic beta-adrenoceptors, activation of adenyl cyclase and consequent increase of the intraneuronal concentration of cAMP. Noradrenaline synthesis in guinea pig atria depolarized by K+ seems to be unrelated to the stimulation of presynaptic adrenoceptors and also independent of the regulation of neurotransmitter release.
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PMID:Presynaptic adrenoceptors on the regulation of tyrosine hydroxylase activation by potassium. 615 72

Isolated dog internal thoracic arteries (ITA) responded to norepinephrine and phenylephrine with concentration-related contractions, which were suppressed by prazosin, but not by yohimbine. Clonidine did not contract ITA. In coronary arterial strips, norepinephrine produced a relaxation. Isoproterenol relaxed coronary arterial strips contracted with serotonin but did not alter the tone of ITA. Forskolin and beraprost, an analog of prostaglandin I2, relaxed coronary and ITA strips to a similar extent. The beta-adrenoceptor density, assayed by [3H]dihydroalprenolol binding, was markedly less in ITA than in coronary arteries. Nicotine and transmural electrical stimulation did not alter the tension of ITA. Immunohistochemical study indicated that nerve fibers containing tyrosine hydroxylase immunoreactivity were markedly less in ITA than in coronary and mesenteric arteries. These results indicate that beta-adrenoceptor function and adrenergic innervation are considerably reduced in dog ITA. Norepinephrine-induced vasocontraction appears to be mediated by alpha 1-adrenoceptors in the arteries.
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PMID:Differences in adrenergic nerve and receptor function in dog internal thoracic, coronary and mesenteric arteries. 772 25

The presence of norepinephrine (NE) and NE activated cells, in the deep cerebellar nuclei (DCN) of male F344 rats, was investigated using immunohistochemistry and electrophysiology, during iontophoresis of the beta-adrenergic agonist isoproterenol (ISO). During extracellular electrophysiology, GABA was iontophoretically applied to the cell and ISO was then co-applied in an attempt to modulate the GABAergic inhibition of cell firing in the DCN. Immunohistochemistry was used to detect tyrosine hydroxylase (TH) positive fibers in the DCN. Isoproterenol modulated GABAergic inhibition in 51% of the DCN cells recorded from. In addition, TH-positive fibers that appeared to make contact with DCN cells were found. Therefore, this study demonstrated that functional NE receptors exist in the DCN and NE appears to be present in fibers therein.
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PMID:Beta-adrenergic modulation of GABAergic inhibition in the deep cerebellar nuclei of F344 rats. 914 43

In the present study, we combined optical Ca(2+) imaging with immunocytochemistry studies to characterize autonomic regulation of Ca(2+) cycling during early development in isolated embryonic mouse hearts. At embryonic days 9.5-11.5 (E9.5-E11.5), the Ca(2+) transient originated in the superior portion of the right atrium, propagated rapidly through both atria, slowly through the atrio-ventricular (AV) ring, and rapidly through both ventricles. Isoproterenol (ISO) significantly increased heart rate, increased Ca(2+) transient amplitude, rate of rise (RR) and a rate of decay, and shortened AV conduction time, indicating the presence of functional beta-adrenergic receptors. The muscarinic agonist carbachol (CCh) had no effects until 1 day later at E10.5. Both beta1-adrenergic and M2 muscarinic receptors were detected in ventricular muscle sections by immunochemistry at E10.5. Growing nerves, labeled using growth-associated protein 43 antibodies, were detected at the E14.5 stage, but not at E10.5, whereas mature sympathetic nerves, detected by tyrosine hydroxylase (TH) labeling, were not yet present at E14.5. These results demonstrate that functional regulation of Ca(2+) cycling by beta-adrenergic receptors occurs earliest in developing embryonic mouse hearts, followed a day later by muscarinic receptor responsiveness, with autonomic innervation developing later. These results define the functional and structural sequence of autonomic regulation of Ca(2+) transient in the embryonic mouse heart.
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PMID:Autonomic regulation of calcium cycling in developing embryonic mouse hearts. 1654 69

The cardiogenic capacity of embryonic stem (ES) cells has been well-investigated. However, little is known about the development of adrenoceptor (AR) systems during the process of ES cell differentiation, which are critically important in cardiac physiology and pharmacology. In this present study, we investigated the expression profile of adrenoceptor subtypes, beta-adrenergic modulation of muscarinic receptors and adrenoceptor-related signaling in cardiomyocytes derived from ES cells (ESCMs). Reverse transcription-polymerase chain reaction revealed that undifferentiated mouse ES cells expressed alpha(1A)-, alpha(1B)-, alpha(1D)- and beta(2)-AR mRNA. However, beta(1)-AR was only expressed after vitamin C induction. The expressions of alpha(1A)-, alpha(1D)- and beta(1)-ARs increased significantly while alpha(1B)- and beta(2)-ARs showed no significant change during the differentiation process. Furthermore, we detected the expression of tyrosine hydroxylase. Both alpha(1)-AR and beta-AR could activate extracellular responsive kinase in ESCMs. Isoprenaline could inhibit the expression of M(2) muscarinic receptor protein. CGP20712A, a beta(1)-AR antagonist, up-regulated the expression of M(2) muscarinic receptor while ICI118551, a beta(2)-AR antagonist, showed no effect. These results indicated that functional adrenoceptors and tyrosine hydroxylase, a critical enzyme in catecholamine biosynthesis, were differentially expressed in ESCMs. Adrenoceptor-related signaling pathways and beta-adrenergic modulation of muscarinic receptors were established during differentiation.
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PMID:Mouse embryonic stem cell-derived cardiomyocytes express functional adrenoceptors. 1827 63