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- _4 wasQuotedFrom 11956243 provenance.
- _4 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" provenance.