The existence of independently functioning local
renin-
angiotensin systems in a number of tissues has been firmly established by biochemical and functional evidence and, most recently, by the demonstration of genetic messages for components of the
renin-
angiotensin systems, such as
renin and
angiotensinogen, in several organs. In this review, local
renin-
angiotensin systems in the heart and vascular walls are described and the contribution of a local inhibition of converting
enzymes to the cardiovascular actions of converting
enzyme inhibitors is discussed. Most of the studies cited support the hypothesis that an inhibition of cardiac converting
enzyme may be involved in the beneficial hemodynamic and metabolic actions of converting
enzyme inhibitors in
cardiovascular disease, such as
hypertension and
congestive heart failure, independent of the circulating renin-angiotensin system. Local effects on cardiac converting
enzyme may contribute to the ability of converting
enzyme inhibitors to reduce
cardiac hypertrophy. Similarly, local converting
enzyme inhibition in the vascular wall may not only constitute a mechanism involved in the
antihypertensive effects of converting
enzyme inhibitors, but may also contribute to the regression of
hypertension-induced vascular
hypertrophy. In addition to reduced local
angiotensin II generation, converting
enzyme inhibition may engender a potentiation of the local effects of
kinins. This mechanism may be more important to the cardiovascular actions of converting
enzyme inhibitors than initially thought.