KININS IN THE CARDIOVASCULAR-SYSTEM

Growing evidence points to the existence of the components of the kall ikrein-kinin-system (KKS) in cardiac and vascular tissue forming syste mic and local KKS pathways involving different cell types like endothe lial cells, cardiomyocytes and vascular smooth muscle cells. Kinins ma y contribute to the regulation of the cardiovascular system in health and disease and to the pharmacological effects of cardiovascular agent s via autocrine-paracrine mechanisms. Based on observations from exper imental models of hypertension, hypertrophy, ischemia, remodelling and preconditioning one can assume that modulation of local KK pathways i s instrumental for endogenous cardio- and vasculoprotective mechanisms . The role of kinins as possible mediators of such protective mechanis ms is not only based on the existence of their generating pathways and their release, but also on observations that kinins, when given local ly or being increased by inhibition of their breakdown, exert benefici al cardiovascular effects, whereas antagonism of their receptors worse ns these effects. Indispensable pharmacological tools like ACE inhibit ors and kinin receptor antagonists have helped to clarify these assump tions, which are now further elucidated by molecular biology and by cl inical research. Especially the wealth of experimental and clinical fi ndings with ACE inhibitors present a continuous challenge to investiga te the role of kinins in the cardiovascular system and to have a close r look at the interdependence of KKS and the Renin-Angiotensin-System (RAS). Within our decade one might not only reach a clearer molecular perception of kinins in the cardiovascular system, and their role in h uman health and disease, but might also come to improved innovative tr eatment by modulation of the KKS pathways.