RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure

The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotensin II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.