The Role of Bradykinin in the Cardiovascular Action of the Converting Enzyme Inhibitor Ramipril [antikvár]

Preface Angiotensin I converting enzyme (ACE) inhibitors were primarily developed as drugs lowering arterial blood pressure by prevention of angiotensin II generation. In pharmacological investigations and clinical studies they exhibit additional local actions which are not related to blood pressure reduction and can not be explained solely by inhibition of the renin-angiotensin system. Potentiation of the kallikrein-kinin systems might be responsible for these additional effects of ACE inhibitors, since ACE is identical to kininase II, the most potent inactivator of kinins. Kinins are to somé extent involved in the blood pressure lowering effect of ACE inhibitors. However, of greater interest for the clinical use of ACE inhibitors are the interactions of kinins with other systems such as prostaglandins, catecholamines and nitric oxidé as well as the cyclic AMP mediated metabolic effects of kinins, by which kinins and, via kinin potentiation, even ACE inhibitors can develop anti-aggregatoric, anti-ischaemic, anti-atnerogenic or energy saving effects. The contributions to this book are focused on the kinin-mediated haemodynamic and metabolic effects of ACE inhibitors and illustrate the most promising perspectives of the new generation of ACE inhibitors like ramipril.