sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_5 ;
    pav:version "20131211" .
  sub:_4 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)" ;
    prov:wasQuotedFrom pubmed:19909806 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:19909806 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}