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The epithelial sodium channel (ENaC), (also known as amiloride-sensitive sodium channel) is a membrane-bound ion channel that is selectively permeable to sodium ions (Na +).It is assembled as a heterotrimer composed of three homologous subunits α or δ, β, and γ, [2] These subunits are encoded by four genes: SCNN1A, SCNN1B, SCNN1G, and SCNN1D.
ENaC is assembled as a heterotrimer composed of three homologous subunits α, β, and γ or δ, β, and γ. The other ENAC subunits are encoded by SCNN1A, SCNN1G, and SCNN1D. [5] ENaC is expressed in epithelial cells [5] and is different from the voltage-gated sodium channel that is involved in the generation of action potentials in neurons ...
In Liddle's syndrome, ENaC-binding potassium-sparing diuretics (e.g. amiloride or triamterene) are used to counter the excess ENaC activity. [4] [10] [2] In AME, the mineralocorticoid receptor-binding potassium-sparing diuretics (e.g. spironolactone or eplerenone) are used to limit aldosterone receptor activity. [1]
n/a Ensembl ENSG00000162572 n/a UniProt P51172 n/a RefSeq (mRNA) NM_001130413 NM_002978 n/a RefSeq (protein) NP_001123885 n/a Location (UCSC) Chr 1: 1.28 – 1.29 Mb n/a PubMed search n/a Wikidata View/Edit Human The SCNN1D gene encodes for the δ (delta) subunit of the epithelial sodium channel ENaC in vertebrates. ENaC is assembled as a heterotrimer composed of three homologous subunits α ...
A mineralocorticoid receptor antagonist (MRA or MCRA) [1] or aldosterone antagonist, is a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure .
The best studied steroid hormone receptors are members of the nuclear receptor subfamily 3 (NR3) that include receptors for estrogen (group NR3A) [1] and 3-ketosteroids (group NR3C). [2] In addition to nuclear receptors, several G protein-coupled receptors and ion channels act as cell surface receptors for certain steroid hormones.
ENaC is assembled as a heterotrimer composed of three homologous subunits α, β, and γ or δ, β, and γ. The other ENAC subunits are encoded by SCNN1A, SCNN1B, and SCNN1D. [5] ENaC is expressed in epithelial cells and is different from the voltage-gated sodium channel that is involved in the generation of action potentials in neurons.
This is a proposed mechanism of aldosterone escape for how patients with increased levels of aldosterone are able to maintain Na + balance and avoid an edematous state. [1] Another mechanism proposed by RW Schrier [6] suggests that aldosterone involves synergistic processes. In addition to increasing renal perfusion pressure, the resultant ...