hyperaldosteronism/tyrosine

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Hyperiodotyrosinemia-induced hyperprolactinemia and hyperaldosteronism.

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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

Modulation of the renin-aldosterone system by iodotyrosines as tyrosine hydroxylase inhibitors.

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This study shows that MIT and DIT stimulate aldosterone secretion. This may be due to their tyrosine hydroxylase inhibitory property. Dopamine abolishes the stimulation. Prolonged MIT administration enhances the stimulation of aldosterone secretion and can cause hypokalemia. Volume expansion

Aldosteronism and peripheral blood mononuclear cell activation: a neuroendocrine-immune interface.

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Aldosteronism eventuates in a proinflammatory/fibrogenic vascular phenotype of the heart and systemic organs. It remains uncertain whether peripheral blood mononuclear cells (PBMCs) are activated before tissue invasion by monocytes/macrophages and lymphocytes, as is the case for responsible

a Novel Y152C KCNJ5 mutation responsible for familial hyperaldosteronism type III.

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BACKGROUND Primary aldosteronism is a heterogeneous group of disorders comprising both sporadic and familial forms. Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III

Transcriptome analysis of primary aldosteronism in adrenal glands and controls.

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Primary aldosteronism (PA) is the most common form of endocrine hypertension. This study was to investigate the gene expression profile in PA adrenal glands and normal controls using RNA-Sequencing. By performing transcriptome analyses for 3 PA adrenal glands and 3 controls on Illumina platform, we

Nintedanib-induced glomerular microangiopathy: a case report.

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Nintedanib, a triple tyrosine kinase inhibitor of vascular endothelial growth factor receptor, platelet-derived growth factor receptor, and fibroblast growth factor receptor, has been used in idiopathic pulmonary fibrosis and adenocarcinoma in advanced non-small cell lung cancer. Although vascular

Fatal neonatal nephrocutaneous syndrome in 18 Roma children with EGFR deficiency.

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Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein with tyrosine-kinase signaling activity, involved in many cellular functions including cell growth and differentiation. Germ line loss-of-function mutations in EGFR lead to a severe neonatal skin disorder (Online Mendelian

Rapid effects of aldosterone on vascular cells: clinical implications.

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Aldosterone has attracted considerable interest as an independent cardiovascular risk marker, which has been demonstrated in a number of studies. Furthermore, recent studies revealed the prevalence of hyperaldosteronism to be about tenfold higher than previously assumed, which underlines its

Receptor binding and biological activity of 18-oxocortisol.

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It has been recently demonstrated that cortisol can be metabolized, producing 18-hydroxycortisol and 18-oxocortisol, following the same pathway by which corticosterone is transformed into 18-hydroxycorticosterone and aldosterone. The influence of a hydroxy group in the 17 alpha position of

Receptor binding and biological activity of 18-hydroxycortisol.

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Recently, 18-hydroxycortisol (11 beta,17 alpha,18,21-tetrahydroxy-4-pregnene-3,20-dione) was isolated and identified from extracts of urine and adrenal incubates of patients with primary aldosteronism. The receptor-binding activity to the renal gluco- and mineralocorticoid receptors and its

Radioimmunoassay of three deoxycorticoids in human plasma following HPLC separation.

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A radioimmunoassay of three deoxycorticoids, namely 11 beta,17 alpha-dihydroxy-4-pregnene-3,20-dione (21-deoxycortisol), 17 alpha,21-dihydroxy-4-pregnene-3,20-dione (11-deoxycortisol), and 21-hydroxy-4-pregnene-3,20-dione (11-deoxycorticosterone) which are important for differential diagnosis of

Effect of dexamethasone on plasma free dopamine: dopaminergic modulation in hypertensive patients.

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To investigate the peripheral dopaminergic modulation in the pathogenesis of human hypertension, we examined the responses of plasma free dopamine (DA) to dexamethasone (Dx) administration, which is suggested to activate dopaminergic activity. We administered Dx 2 mg intravenously to patients with

Plasma free dopamine: physiological variability and pathophysiological significance.

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Dopamine (DA) is the most abundant catecholamines in human plasma and exists mostly in the sulfo-conjugated form (DA sulfate), a biologically inactive metabolite. The paucity of unconjugated DA (PDA) in plasma throws doubt on its physiological significance. However, PDA, when measured with a highly

Regulation of aldosterone synthesis and secretion.

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Aldosterone is a steroid hormone synthesized in and secreted from the outer layer of the adrenal cortex, the zona glomerulosa. Aldosterone is responsible for regulating sodium homeostasis, thereby helping to control blood volume and blood pressure. Insufficient aldosterone secretion can lead to

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