Markus Magerl, Michael Bader, Anne Gompel, Kusumam Joseph, Allen P. Kaplan, Georg Kojda, Thomas Renné, Markus Wirth, Marcus Maurer, Martin K. Church
The following summarises the plenary lectures of the ‘Bradykinin Symposium 2012’ held on 23−24 August 2012 at Charité-Universitätsmedizin Berlin, Germany. The summary begins with bradykinin activation, examines the effects of bradykinin in different organs of the body, provides an update on the role and regulation of bradykinin receptors, introduces the effects of oestrogens on bradykinin-mediated angioedema and concludes with models that may lead to new therapies.
Bradykinin activation (A.P. Kaplan, Charleston, USA) Activation of the plasma bradykinin-forming cascade
The plasma constituents of the bradykinin-forming cascade consist of factor XII, prekallikrein, and high-molecular-weight kininogen (HK). Although each protein is a separate gene product, prekallikrein circulates bound to HK, i.e., 70–75 % exist as a bimolecular complex while 25–30 % of prekallikrein is free. Traditional ‘contact’ activation begins with addition of a negatively charged surface which can be inorganic.