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 "# Pubmed:gene: Increased vascular permeability in C1 inhibitor-deficient mice mediated by the bradykinin type 2 receptor. This increased vascular permeability was reversed by treatment with intravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor (DX88), and with a bradykinin type 2 receptor (Bk2R) antagonist (Hoe140).  In addition, treatment of the C1INH-deficient mice with an angiotensin-converting enzyme inhibitor (captopril) increased the vascular permeability. Bradykinin is a small peptide vasodilator formed in blood and tissue fluids by cleavage of alpha2-globulins. It causes both arteriolar dilation and increased capillary permeability" ;
    prov:wasQuotedFrom pubmed:11956243 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:11956243 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}