Role of the cardiac renin-angiotensin system in hypertensive cardiac hypertrophy.

The unique efficacy of converting-enzyme inhibitors in inducing regression, or preventing the occurrence, of ventricular hypertrophy associated with systemic hypertension has for many years pointed to a possible direct effect of the renin-angiotensin system in the pathogenesis of cardiac hypertrophy. Over the last 10 years evidence has been forthcoming about direct trophic effects of angiotensin II in several experimental systems, and we now have conclusive evidence for the existence of a local, intracardiac renin-angiotensin system. This system is capable of local synthesis of all components of the renin-angiotensin system, and has been demonstrated to be capable to cleave, via the classic pathway, angiotensin peptides from the precursor, angiotensinogen. Moreover, a number of studies have demonstrated the capacity of regulatory response and modulation of activity of the local system in response to a variety of pharmacological perturbations, and differential regulation of expression of specific components under pathological conditions. There is, thus, fairly solid evidence for participation of the cardiac renin-angiotensin system in the pathogenesis of hypertensive cardiac hypertrophy. Whether this participation is causative in character, or only a secondary event, and what precisely are the stimuli that modulate the activity of the cardiac renin-angiotensin system, are questions that are still poorly understood, but being actively researched.