Bradykinin may mediate the effects of ACE inhibitors on endothelial function, ischemic hearts, cardiac hypertrophy, and myocardial capillary growth via paracrine-autocrine mechanisms.
Antihypertensive drugs interfering with the renin-angiotensin system, such as angiotensin converting enzyme inhibitors are increasingly discussed with respect to their effects beyond blood pressure control, for instance on vascular and cardiac structure and function. ACE inhibitors which not only prevent the conversion of angiotensin I to angiotensin II but also the degradation of bradykinin (BK), may exert their actions in part via paracrine-autocrine mechanisms including the kallikrein-kinin system. In a short review we will describe the effects of BK on endothelial function, on ischaemic hearts and cardiac hypertrophy and discuss a possible involvement of BK in myocardial capillary growth after ACE inhibition.
Tschöpe et al. (Sun,) conducted a review in Hypertension / Cardiac hypertrophy / Ischaemic heart disease. ACE inhibitors / Bradykinin was evaluated. Bradykinin may mediate the effects of ACE inhibitors on endothelial function, ischemic hearts, cardiac hypertrophy, and myocardial capillary growth via paracrine-autocrine mechanisms.