Role of bradykinin in preconditioning and protection of the ischaemic myocardium

Angiotensin Receptor Blockers May Increase Risk of Myocardial Infarction

“…54 Bradykinin is also a key mediator of ischemic preconditioning, a unique cytoprotective phenomenon that allows myocardial cells to withstand injury from prolonged exposure to ischemia if first exposed to repeated brief bouts of ischemia. 55 Ischemic preconditioning can limit both infarct size and ischemia-mediated ventricular arrhythmias 55 and may contribute to the vascular protective effects of ACEIs. The relative lack of effect of ARBs on bradykinin may limit the aforementioned effects.…”

Ischemic Preconditioning Attenuates Postischemic Leukocyte - Endothelial Cell Interactions Role of Nitric Oxide and Protein Kinase C

“…19 Numerous attempts have been made to elucidate the mechanisms behind preconditioning, but results have suggested nearly as many possible mediators as there have been attempts. These possible mediators include NO, 20 acetylcholine, 21 catecholamines, 22 angiotensin II, 23 bradykinin, 24 adenosine, 25 and reactive oxygen species (ROS). 26,27 Although the roles of NOS/NO and PKC in IPC in the heart and many other organs have been extensively discussed, [28][29][30] only few studies have investigated skeletal muscle [31][32][33] and the microcirculatory leukocyte-endothelium interaction.…”

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

“…Second, experimental ischemic preconditioning, perhaps with multiple cycles of ischemia, recruits multiple autacoid mediators whereas a pharmacological preconditioning "mimetic" may rely on the manipulation of a single autacoid system. For example, the experimental infarct-limiting effects of ACE inhibitors may be in large part due to inhibition of kinin degradation (for a review, see Baxter and Ebrahim, 2002), and the acute infarctlimiting effect of statins, independent of serum cholesterol lowering, appears to be due to enhanced NO biosynthesis via promotion of PI3K/Akt signaling (Bell and Yellon, 2003b;Wolfrum et al, 2003;Elrod and Lefer, 2005). Yet, in hypertension, as in other cardiovascular diseases, a generalized endothelial dysfunction occurs (Drexler and Hornig, 1999); this dysfunction may extend to the myocardium itself where there is a reduction in the capacity of hypertrophied myocardium to synthesize NO (MacCarthy and Shah, 2000;Pacher et al, 2005).…”