Authors: D J Campbell A Kladis Y Zhang A J Jenkins D L Prior M Yii J F Kenny M J Black D J Kelly
Publish Date: 2010/01/10
Volume: 53, Issue: 4, Pages: 779-785
Abstract
Circulating levels of bradykinin and kallidin peptides and high and low molecular weight kininogens as well as plasma and tissue kallikrein and kallistatin were measured in nondiabetic and diabetic patients before coronary artery bypass graft surgery Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantifiedPlasma levels of tissue kallikrein were approximately 62 higher in diabetic than in nondiabetic patients p = 0001 whereas no differences were seen in circulating levels of bradykinin and kallidin peptides and high and low molecular weight kininogens or in plasma kallikrein or kallistatin Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes p = 0015 while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients p = 0014 Statin therapy did not change any variables of the circulating kallikrein–kinin system Neither aspirin calcium antagonists beta blockers or longacting nitrate therapies influenced any kallikrein–kinin system variableTissue kallikrein levels are increased in type 2 diabetes whereas statin therapy does not modify the circulating kallikrein–kinin system Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in nondiabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients However our findings do not support a role for the kallikrein–kinin system in mediating the effects of statin therapy on endothelial function
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