essential hypertension/tyrosine

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Effect of pyratrione (a tyrosine hydroxylase inhibitor) in essential hypertension.

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1. A clinical study of pyratrione, a tyrosine hydroxylase inhibitor, has been carried out in essential hypertension. 2. Out of thirty-nine patients who received pyratrione, twenty-eight showed a significant decrease in blood pressure.

[Genetic polymorphism in tyrosine hydroxylase gene and essential hypertension in Hunan Han population].

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OBJECTIVE To investigate the association of tyrosine hydroxylase (TH) C-824T polymorphism with essential hypertension (EH) susceptibility in Hunan Han population by a case-control study. METHODS A case-control study was performed on 368 EH patients and 353 healthy controls of Han nationality

A functional intronic variant in the tyrosine hydroxylase (TH) gene confers risk of essential hypertension in the Northern Chinese Han population.

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The TH (tyrosine hydroxylase) gene encodes the rate-limiting enzyme of catecholamine biosynthesis, and is involved in the pathogenesis of hypertension, but the relationship of its variants with hypertension has not been extensively studied. We designed a case-controlled study consisting of 503 HT

Positive association of tyrosine hydroxylase microsatellite marker to essential hypertension.

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Despite advances in the understanding of monogenic hypertensive disorders, the genetic contribution to essential hypertension has yet to be elucidated. The position of tyrosine hydroxylase (TH) as the rate-limiting enzyme in catecholamine biosynthesis renders it a candidate gene for the etiology of

Chronic dietary tyrosine supplements do not affect mild essential hypertension.

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The blood pressure and plasma norepinephrine response to oral tyrosine, the precursor of norepinephrine, supplementation (2.5 g t.i.d.) of regular meals was examined in 13 untreated patients with mild essential hypertension. Using a randomized double-blind crossover design, each 2-week treatment was

Bisoprolol and captopril effects on insulin receptor tyrosine kinase activity in essential hypertension.

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Angiotension converting enzyme (ACE) inhibitors and beta-blockers have been reported to possess disparate effects on insulin sensitivity. The aim of this study was to study the effects of the selective beta-1 blocker bisoprolol and of the ACE inhibitor captopril on cellular insulin action in

Protein tyrosine phosphatase 1B gene polymorphisms and essential hypertension: a case-control study in Chinese population.

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BACKGROUND Protein tyrosine phosphatase (PTP)- 1B, encoded by the PTPN1 gene, negatively regulates insulin signaling by dephosphorylating the phosphotyrosine residues of the insulin receptor kinase activation segment. Several rare single nucleotide polymorphisms (SNP) have been linked to diseases

Single nucleotide polymorphisms in protein tyrosine phosphatase 1beta (PTPN1) are associated with essential hypertension and obesity.

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Protein tyrosine phosphatase 1beta (PTP-1beta) is involved in the regulation of several important physiological pathways. It regulates both insulin and leptin signaling, and interacts with the epidermal- and platelet-derived growth factor receptors. The gene is located on human chromosome 20q13, and

[ISOLATION AND PREPARATION IN A PURE STATE OF THE ENZYME L-TYROSINE-HYDROXYLASE IMPORTANT IN ESSENTIAL HYPERTENSION].

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Increased migration of monocytes in essential hypertension is associated with increased transient receptor potential channel canonical type 3 channels.

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Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed

Protein tyrosine kinase 2beta as a candidate gene for hypertension.

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Protein tyrosine kinase 2beta (PTK2B) is a member of the focal adhesion kinase family and is activated by angiotensin II through Ca2+-dependent pathways. An evidence exists that PTK2B is involved in cell growth, vascular contraction, inflammatory responses, and salt and water retention through

Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension.

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One of the major pathophysiological features of primary hypertension is an inappropriate activation of the sympathetic nervous system, which is mediated by excessive synthesis and secretion of catecholamine into the blood. Tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of

Association analysis of two tyrosine hydroxylase gene polymorphisms in normotensive offspring from hypertensive families.

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OBJECTIVE We have studied possible association between predisposition to essential hypertension, plasma noradrenaline level and two polymorphisms of the gene for tyrosine hydroxylase (TH), the rate-limiting enzyme of catecholamine biosynthesis. METHODS One hundred and one normotensive sons from

Biochemical evaluation of sympathetic nerve tone in essential hypertension.

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The concentration of plasma catecholamines (CA), serum dopamine beta-hydoxylase (DBH) activity and plasma renin activity (PRA) were simultaneously measured in 55 patients with essential hypertension (EH). Further the enzyme activities of CA biosynthesis in human vas deferens excised at elective

TH01, a tetrameric short tandem repeat locus in the tyrosine hydroxylase gene: association with myocardial hypertrophy and death from myocardial infarction?

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TH01 is a tetrameric short tandem repeat locus located in intron 01 of the tyrosine hydroxylase gene. The tyrosine hydroxylase catalyzes the hydroxylation of L-tyrosine to L-DOPA and is the rate limiting enzyme in the synthesis of catecholamines like noradrenaline or adrenaline, which are pivotal in

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