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

Discrete brain areas and sympathetic ganglia obtained at autopsy from patients with idiopathic orthostatic hypotension were assayed for tyrosine hydroxylase and dopamine beta-hydroxylase. Dopamine beta-hydroxylase activity was decreased 7.5-fold in sympathetic ganglia, while tyrosine hydroxylase activity was reduced more than 50-fold in the pontine nucleus locus coeruleus. These observations indicate that noradrenergic neurons of both brain and ganglion are affected in idiopathic orthostatic hypotension, but suggest that the central and peripheral biochemical deficits differ.
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PMID:Catecholamine enzymes in the degenerative neurological disease idiopathic orthostatic hypotension. 0 74

Reserpine (1 mg/kg) was administered to pregnant rats on days 12, 13 and 14 of gestation. Although adrenal tyrosine hydroxylase and dopamine beta-hydroxylase activities were normal in the offspring at 4 days of postnatal age, both were elevated by 17 days and the elevations persisted into adulthood. The changes may result from permanently increased sympatho-adrenal stimulation.
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PMID:Prenatal reserpine administration: permanent changes in adrenal tyrosine hydroxylase and dopamine beta-hydroxylase. 0 1

Three litters of pigs were weaned at 21 days of age, and 3 others were left with the sow. Pigs were killed at 21, 23, 28, or 39 days of age. Weaned pigs exhibited anxiety, gastrointestinal dysfunction, and decreased rate of body weight gain. Plasma glucose or liver glycogen concentrations were not decreased by weaning. Adrenal gland weights and tyrosine hydroxylase (EC 1.14.3a), dopamine beta-hydroxylase (EC 1.14.2.1), phenethanolamine-N-methyl transferase (EC 2.1.1), and monoamine oxidase (EC 1.4.3.4) activities were increased after weaning. Adrenal catecholamine and cortisol levels and dopa decarboxylase (EC 4.1.1.26) and catechol-o-methyl transferase (EC 2.1.1.6) activities were not significantly altered, although some increases were indicated. Cranial cervical ganglionic choline acetyltransferase (EC 2.3.1.6) and tyrosine hydroxylase activities were increased after weaning. Weaning of swine at 21 days of age is a stressful experience, and many effects persist for at least 18 days; however, growth was no longer impaired 18 days after weaning.
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PMID:Sympathoadrenal Neurochemistry and early weaning of swine. 0 71

It was the aim of the present study to elucidate the mechanisms involved in specific tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) induction by potassium depolarization and cholinomimetics in rat superior cervical ganglia kept in organ culture. The effect of high (54 mM) potassium concentration on intact ganglia seems to result in a dual action: a) a specific induction of TH and DBH via release of acetylcholine from preganglionic cholinergic nerve terminals. b) a non-specific effect on terminal adrenergic neurons resulting in a general increase of protein synthesis as indicated by the increase in DOPA decarboxylase (DDC) and monoamine oxidase (MAO) activities. In decentralized superior cervical ganglia potassium depolarization failed to produce the specific TH and DBH induction although a small increase in DDC activity persisted. Carbamylcholine, acetylcholine and nicotine at concentrations of 10(-4) M elicited a selective induction of TH and DBH both in intact and decentralized ganglia via nicotinic receptor stimulation. Bethanechol, predominantly stimulating muscarinic receptors had no significant effect on TH activity. A 4 h pulse of 10(-4) M carbamylcholine produced optimal induction of DBH and TH 24 h and 48 h later respectively. Longer exposure to carbamylcholine resulted in a significantly smaller rise in TH activity.
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PMID:Mechanisms of tyrosine hydroxylase and dopamine beta-hydroxylase induction in organ cultures of rat sympathetic ganglia by potassium depolarization and cholinomimetics. 0 52

By use of a sensitive and specific enzymatic isotopic method for the determination of tyramine, the small quantities of this amine which are present endogenously in rat tissues, including brain, heart, kidney and salivary gland, have been quantitated. The levels of tyramine in brain were increased to a similar extent by injecting animals with a monoamine oxidase inhibitor, pargyline, and a dopamine beta-hydroxylase inhibitor, FLA-63; in contrast, pretreatment of animals with alpha-methyl-para-tyrosine, a tyrosine hydroxylase inhibitor, did not lead to an increase in tyramine levels in brain. Pretreatment of rats with 6-hydroxydopamine resulted in a marked diminution in the tyramine content of rat atria and salivary gland. Denervation of the salivary gland decreased the endogenous level of tyramine approximately 50% in denervated glands compared to undenervated glands. These results suggest that tyramine exists at least partly in sympathetic nerves in many tissues.
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PMID:Biosynthesis and metabolism of endogenous tyramine and its normal presence in sympathetic nerves. 1 Apr 24

The activities of tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), dopamine beta-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT), and monoamine oxidase (MAO) with serotonin and phenylethylamine as substrates were measured in catecholaminergic regions of human brain from 10 controls and 3 patients with Parkinsonism. PNMT activity was detected in hypothalamus, thalamus and cerebellar nucleus of the control human brain, and was reduced in hypothalamus of Parkinsonian cases. Type A (with serotonin as substrate) and type B (with phenylethylamine as substrate) MAO activities were high in all brain regions with little individual variations in controls and Parkinsonian cases. TH activity was high in the controls and was markedly decreased, in substantia nigra, caudate nucleus, putamen and in pallidum, in all three cases of Parkinsonism. DDC activity in these regions was also decreased in 2 patients. However, one Parkinsonian case had only decreased TH and normal DDC activities. DBH activity in hypothalamus was also reduced in the Parkinsonian cases.
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PMID:Phenylethanolamine N-methyltransferase and other enzymes of catecholamine metabolism in human brain. 1 98

The centrally active muscarinic agonist, oxotremorine, elicited an up to 2-fold dose-dependent (0.25-1.5 mg/kg) increase in the activity of tyrosine hydroxylase (TH) in the rat nucleus locus coeruleus (LC) and adrenal medulla. The response occurred in LC after 24 to 48 hours and in adrenal medulla by 4 to 8 hours, peaked in LC at 72 hours and adrenal medulla at 16 to 24 hours and persisted up to 2 weeks in both tissues. In brain the effect appeared confined to cell bodies of noradrenergic neurons. The activity of dopamine beta-hydroxylase increased in adrenal medulla (40%) but not in brain. Immunotitration with anti-TH serum demonstrated that the increase of TH activity in LC is due to increased catalytic activity (activation), whereas in adrenal medulla it is due to a transynaptically mediated accumulation of enzyme protein (induction). Physostigmine (1.0 mg/kg), pilocarpine (25-50 mg/kg) and nicotine (10 mg/kg) increased TH activity in LC and adrenal. We conclude that stimulation of central cholinergic receptors of the muscarinic type results in a delayed and protracted activaiton of TH but not of dopamine beta-hydroxylase in cell bodies of central noradrenergic neurons, and reflexly, to transynaptic induction of TH and dopamine beta-hydroxylase in the adrenal medulla.
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PMID:Tyrosine hydroxylase: delayed activation in central noradrenergic neurons and induction in adrenal medulla elicited by stimulation of central cholinergic receptors. 1 97

1. The development of nicotinic responses in the rat adrenal medulla was examined at various ages from 1 to 50 days of age by testing the ability of nicotine (10 mg/kg, s.c.) to deplete catecholamines and induce tyrosine hydroxylase. 2. Catecholamines were depleted 25% 3 h after injection of nicotine at all ages tested, but the degree of tyrosine hydroxylase induction 24 h after nicotine increased with age. 3. These data indicate that functional nicotinic receptors are present in the neonatal adrenal medulla before the development of functional splanchnic innervation, but that the development of the ability to induce tyrosine hydroxylase is not coupled directly to the development of secretory mechanisms. 4. The long-term effects of a single dose of nicotine (10 mg/kg, s.c.) administered to one day old rats were also examined. 5. After the short-term catecholamine depletion caused by nicotine, there were persistent elevations of catecholamines and tyrosine hydroxylase until 23 days of age; however, dopamine beta-hydroxylase remained elevated into young adulthood. 6. These data indicate that neonatal nicotine administration can produce long-term changes in adrenal catecholamine biosynthetic enzymes.
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PMID:Development of nicotinic responses in the rat adrenal medulla and long-term effects of neonatal nicotine administration. 1 46

In young, spontaneously hypertensive rats (SHR), a preganglionic, nerve-dependent, elevation of choline acetyltransferase (ChAc) and tyrosine hydroxylase (TH) activities was found in celiac ganglia as compared with those in young, normotensive Kyoto Wistar rats, that was not present in superior cervical ganglia, stellate ganglia and adrenal glands. The rise in both enzyme activities in the celiac ganglion disappeared in adult SHR. An elevation of plasma norepinephrine and dopamine beta-hydroxylase levels found in prehypertensive SHR, a probable indication of peripheral sympathetic activation, disappeared after the bilateral removal of the celiac ganglion. However, ganglionectomy did not change the subsequent development of hypertension. These results indicate that the faster maturation of the celiac ganglion and the end organs it innervates in yount SHR are causally related to the activation of the peripheral sympathetic nervous system. The peripheral sympathetic activation in young SHR is regarded as a warning sign but this does not trigger the development of hypertension.
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PMID:Enhanced sympathetic activity in young spontaneously hypertensive rats is not the trigger mechanism for genetic hypertension. 2 May 86

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II). 2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks. 3. Hypothalamic tyrosine hydroxylase and dopamine beta-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks. 4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.
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PMID:Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. 3


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