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References in periodicals archive ?
This hypothesis is focused on the C-2399A polymorphism because previous studies have shown that this SNP reduces APP activity and thereby potentially prolongs the half-life of bradykinin and/or its active metabolites.
During normal contact activation (caused by tissue damage), activated factor 12 cleaves prekallikrein to kallikrein which then leads to bradykinin formation.
Typical examples of cross talk in such factors include bradykinin by inducing cyclooxygenase (COX) II, and eNOS activation (30-32,34,35) These cytokines cross talk each other and affect vascular tone.
Bradykinin (BK) is known for its proinflammatory functions in both tissue injury and allergic inflammation of the airway mucosa.
The frequent reaction of hypotension has been speculated to result from the use of angiotensin-converting enzyme (ACE) inhibitors when using 5% albumin as the replacement fluid due to an accumulation of bradykinin, a vasodilator which causes hypotension.
Either the absence of or a defect in the C1-INH-complement-system inhibitor results in uncontrolled regulation of the complement, kallikrein, and bradykinin systems (Starr, Brasher, Arundhati, & Posey, 2004).
activate proinflammatory mediators such as bradykinin.
Bradykinin also stimulates the release of prostaglandins and substance p, a potent neurotransmitter that enhances movement of impulses across synapses.
Steroids and antihistamines are ineffective as the mechanism of the reaction is not allergic but related to bradykinin.
1-3) Angioedema due to ACE inhibitors appears to be linked to the decreased degradation of bradykinin because ACE, also known as kininase II, not only activates angiotensin I but also inactivates bradykinin.
The researchers also found that bronchoconstriction was reduced by 34% when animals were treated with HOE-140, a bradykinin [[beta].