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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#_4 http://www.w3.org/ns/prov#value When aldosterone enters the cell, it binds to the mineralocorticoid receptor (MR), and thereafter the ligand-receptor complex is translocated into the nucleus. Binding to hormone response elements (HRE) increases the transcription of genes encoding specific aldosterone-inducible proteins, such as rate-limiting subunits of the apical epithelial sodium channel (ENaC) (Fig. 1A). In response sodium influx causes intracellular sodium (Na+) to rise; this increase in substrate increases turnover of Na+/K+ ATPase, which in turn increases Na+ reabsorption and potassium (K+) excretion. Activation and induction of these Na+ transporters is crucial to unfold the physiological role of the aldosterone system, which is to counteract excessive water and salt loss and maintain normotension in the face fluid losses. On the other hand, unrestrained activation of the MR, as occurs in many forms of mineralocorticoid hypertension, causes excessive Na+ reabsorption leading to volume expansion and contributes to hypertension. (See Figure 1. Note: Will change to ENaC Complex Hs once term is created -JP) http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#_4 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/19909806 http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#_5 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/19909806 http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#_4 http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8#pubinfo http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8 http://purl.org/dc/terms/created 2014-07-03T14:30:55.167+02:00 http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8 http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RALqDtoJz5FWBBy78ouw5vayAUS-tTZI9aTh1M5qtgfj8 http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234