Concentrating defect in experimental nephrotic syndrone: altered expression of aquaporins and thick ascending limb Na+ transporters.
about
Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expressionShort-term functional adaptation of aquaporin-1 surface expression in the proximal tubule, a component of glomerulotubular balance.The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenonAcute hypertension provokes internalization of proximal tubule NHE3 without inhibition of transport activityRegulation and dysregulation of aquaporins in water balance disorders.Sex differences in adaptive downregulation of pre-macula densa sodium transporters with ANG II infusion in mice.Aldosterone-mediated regulation of ENaC alpha, beta, and gamma subunit proteins in rat kidney.Upregulation of renal sodium transporters in D5 dopamine receptor-deficient mice.Regulation of aquaporins and sodium transporter proteins in the solitary kidney in response to partial ureteral obstruction in neonatal rats.mPGES-1 deletion impairs aldosterone escape and enhances sodium appetiteIncreased renal alpha-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy.Erlotinib preserves renal function and prevents salt retention in doxorubicin treated nephrotic rats.Protein abundance of urea transporters and aquaporin 2 change differently in nephrotic pair-fed vs. non-pair-fed rats.Targeted proteomics using immunoblotting technique for studying dysregulation of ion transporters in renal disorders.Aquaporin 2 promotes cell migration and epithelial morphogenesis.NF-kappaB modulates aquaporin-2 transcription in renal collecting duct principal cells.Vasopressin and the regulation of aquaporin-2Absence of renal enlargement in fructose-fed proximal-tubule-select insulin receptor (IR), insulin-like-growth factor receptor (IGF1R) double knockout mice.Animal models of nephrotic syndrome.Dynamic regulation and dysregulation of the water channel aquaporin-2: a common cause of and promising therapeutic target for water balance disorders.Absence of aquaporin-4 water channels from kidneys of the desert rodent Dipodomys merriami merriami.Inhibition of the renal betaine transporter by calcium ions.Ezrin binding domain-deficient NHERF attenuates cAMP-mediated inhibition of Na(+)/H(+) exchange in OK cells.Rosiglitazone prevents sirolimus-induced hypomagnesemia, hypokalemia, and downregulation of NKCC2 protein expression.Compensatory increase in AQP2, p-AQP2, and AQP3 expression in rats with diabetes mellitus.Altered expression of renal aquaporins and Na(+) transporters in rats treated with L-type calcium blocker.Effects of receptor-mediated endocytosis and tubular protein composition on volume retention in experimental glomerulonephritis.Time course of renal Na-K-ATPase, NHE3, NKCC2, NCC, and ENaC abundance changes with dietary NaCl restriction.Sodium transporter abundance profiling in kidney: effect of spironolactone.Altered expression of renal NHE3, TSC, BSC-1, and ENaC subunits in potassium-depleted rats.Effect of primary polydipsia on aquaporin and sodium transporter abundance.Increased renal ENaC subunit and sodium transporter abundances in streptozotocin-induced type 1 diabetes.Na+-H+ exchange activity in taste receptor cells.Effects of dietary fat, NaCl, and fructose on renal sodium and water transporter abundances and systemic blood pressure.COX-2 inhibition prevents downregulation of key renal water and sodium transport proteins in response to bilateral ureteral obstruction.NKCC1 and NHE1 are abundantly expressed in the basolateral plasma membrane of secretory coil cells in rat, mouse, and human sweat glands.Nonosmotic release of vasopressin and renal aquaporins in impaired urinary dilution in hypothyroidism.Increased apical targeting of renal ENaC subunits and decreased expression of 11betaHSD2 in HgCl2-induced nephrotic syndrome in rats.Increased expression but not targeting of ENaC in adrenalectomized rats with PAN-induced nephrotic syndrome.Increased renal alpha-ENaC and NCC abundance and elevated blood pressure are independent of hyperaldosteronism in vasopressin escape.
P2860
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P2860
Concentrating defect in experimental nephrotic syndrone: altered expression of aquaporins and thick ascending limb Na+ transporters.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh-hant
name
Concentrating defect in experi ...... cending limb Na+ transporters.
@en
Concentrating defect in experi ...... cending limb Na+ transporters.
@nl
type
label
Concentrating defect in experi ...... cending limb Na+ transporters.
@en
Concentrating defect in experi ...... cending limb Na+ transporters.
@nl
prefLabel
Concentrating defect in experi ...... cending limb Na+ transporters.
@en
Concentrating defect in experi ...... cending limb Na+ transporters.
@nl
P2093
P1433
P1476
Concentrating defect in experi ...... cending limb Na+ transporters.
@en
P2093
Ecelbarger CA
Fernández-Llama P
P304
P356
10.1046/J.1523-1755.1998.00984.X
P407
P577
1998-07-01T00:00:00Z
P5875
P6179
1041890832