[Role of the cardiac renin-angiotensin system in hypertensive heart disease].

Chronic mechanical stress of the heart by arterial hypertension is a primary cause of left ventricular hypertrophy. The cardiac renin-angiotensin system is often found activated in conditions of increased afterload or mechanical stress of myocytes. Cardiac expression of angiotensinogen and angiotensin-converting enzyme (ACE) is increased resulting in elevated cardiac angiotensin II formation. This has been demonstrated in stretched cardiac myocytes in vitro as well as in animal models of pressure overload hypertrophy (supravalvular aortic stenosis and spontaneously hypertensive rats) and in human pressure overload hypertrophy (aortic stenosis). Functional consequences of elevated angiotensin II levels may be vasoconstriction of the coronary vasculature and a deterioration of diastolic function of the hypertrophied heart. Local formation of angiotensin II may also have proliferative effects on cardiac myocytes and connective tissue cells. Angiotensin II may, thus, be an important factor causing development and progression of left ventricular hypertrophy by itself. Blockade of the renin-angiotensin system has been found to be an effective treatment of hypertensive heart disease, probably better than any other antihypertensive medication. Regression of left ventricular hypertrophy has been achieved by blockade of the angiotensin II pathway either by administration of an angiotensin-converting enzyme inhibitor or an angiotensin II type 1-receptor blocker. The animal model of supravalvular aortic stenosis has been used to show beneficial effects of blockade of the renin-angiotensin system on hypertrophy and survival. In this rat model regression of left ventricular hypertrophy by ACE-inhibition or angiotensin II type 1-receptor blockade could be demonstrated by serial echocardiographic analyses while afterload of the left ventricle was still elevated.(ABSTRACT TRUNCATED AT 250 WORDS)