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15 resultater
Consequences of SPAK inactivation on Hyperkalemic Hypertension caused by WNK1 mutations: evidence for differential roles of WNK1 and WNK4.
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Mutations of the gene encoding WNK1 [With No lysine (K) kinase 1] or WNK4 cause Familial Hyperkalemic Hypertension (FHHt). Previous studies have shown that the activation of SPAK (Ste20-related Proline/Alanine-rich Kinase) plays a dominant role in the development of FHHt caused by WNK4 mutations.
Molecular genetics of Liddle's syndrome.
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Liddle's syndrome, an autosomal dominant form of monogenic hypertension, is characterized by salt-sensitive hypertension with early penetrance, hypokalemia, metabolic alkalosis, suppression of plasma rennin activity and aldosterone secretion, and a clear-cut response to epithelial sodium channel
Endotoxin-neutralizing effects of histidine-rich peptides.
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Inflammatory responses of human peripheral blood monocytes to the Gram-negative endotoxin lipopolysaccharide (LPS) are enhanced by structurally diverse substances, such as anionic polysaccharides or cationic polypeptides. Only a few substances are known to effectively blunt LPS-induced monocyte
Analysis of claudin genes in pediatric patients with Bartter's syndrome.
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Bartter's syndrome is a constellation of symptoms characterized by hyper-reninemic hypokalemia, metabolic alkalosis, elevated renin and aldosterone, low or normal blood pressure, and hyperplasia of the juxtaglomerular apparatus. So far, five gene mutations in proteins regulating the sodium chloride
NH3- and CO2-induced suppression of taste nerve responses in clawed toads and eels.
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We investigated the effects of intracellular pH values (pHi) on taste nerve responses of clawed toads and eels. (1) CO2, NH3 or trimethylamine reversibly suppressed the taste nerve responses of clawed toads to various amino acids, CaCl2 and caffeine. IC50 values of the suppression of the responses
The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney.
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Kir4.1 is an inwardly rectifying potassium (K(+)) channel and is expressed in the brain, inner ear, and kidney. In the kidney, Kir4.1 is expressed in the basolateral membrane of the late thick ascending limb (TAL), the distal convoluted tubule (DCT), and the connecting tubule (CNT)/cortical
Modulation of NCC activity by low and high K(+) intake: insights into the signaling pathways involved.
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Modulation of Na(+)-Cl(-) cotransporter (NCC) activity is essential to adjust K(+) excretion in the face of changes in dietary K(+) intake. We used previously characterized genetic mouse models to assess the role of Ste20-related proline-alanine-rich kinase (SPAK) and with-no-lysine kinase (WNK)4 in
Stability of amino acids and the availability of acid in total parenteral nutrition solutions containing hydrochloric acid.
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The stability of amino acids and the availability of acid from total parenteral nutrition (TPN) solutions containing hydrochloric acid were studied. Hydrochloric acid in the concentrations of 40 (TPN 1), 60 (TPN 2), and 100 (TPN 3) meq/liter was added to TPN solutions (4.25% amino acids, 25%
Effects of gas composition and pH on kinetics of lung angiotensin-converting enzyme.
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Given the pH dependence of enzymes in general and the potential importance of a blood and alveolar gas composition dependency on the interpretation of changes in the hydrolysis of angiotensin-converting enzyme (ACE) substrates by pulmonary endothelial ACE, we examined the influence of Pco2 and Po2
pH sensors and ion Transporters: Potential therapeutic targets for acid-base disorders.
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Regulation of pH is critical for physiological processes. Maintenance of acid-base homeostasis is tightly regulated by the renal and respiratory systems. However, fluctuations in extracellular pH are also sensed by other organ systems. Ion transporter activity to modify the amount of acid (H+ and
Late-onset ornithine transcarbamylase deficiency in male patients: prognostic factors and characteristics of plasma amino acid profile.
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BACKGROUND
The occurrence of male patients with ornithine transcarbamylase (OTC) deficiency during adolescence or in adulthood has now been recognized. The aim of this study was to determine the prognostic factors that affect the prognosis of life, to explore a basis for therapeutic
A genetic defect resulting in mild low-renin hypertension.
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Severe low-renin hypertension has few known causes. Apparent mineralocorticoid excess (AME) is a genetic disorder that results in severe juvenile low-renin hypertension, hyporeninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thrive, poor growth, and in many cases
The WNK-SPAK/OSR1 Kinases and the Cation-Chloride Cotransporters as Therapeutic Targets for Neurological Diseases.
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In recent years, cation-chloride cotransporters (CCCs) have drawn attention in the medical neuroscience research. CCCs include the family of Nap>+ p>-coupled Clp>- p> importers (NCC, NKCC1, and NKCC2), Kp>+ p>-coupled Clp>- p> exporters (KCCs), and possibly polyamine
Argininosuccinate lyase deficiency-argininosuccinic aciduria and beyond.
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The urea cycle consists of six consecutive enzymatic reactions that convert waste nitrogen into urea. Deficiencies of any of these enzymes of the cycle result in urea cycle disorders (UCD), a group of inborn errors of hepatic metabolism that often result in life threatening hyperammonemia.
KCNJ10 determines the expression of the apical Na-Cl cotransporter (NCC) in the early distal convoluted tubule (DCT1).
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The renal phenotype induced by loss-of-function mutations of inwardly rectifying potassium channel (Kir), Kcnj10 (Kir4.1), includes salt wasting, hypomagnesemia, metabolic alkalosis and hypokalemia. However, the mechanism by which Kir.4.1 mutations cause the tubulopathy is not completely understood.
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