[Role of the cardiac renin-angiotensin system in XXXX ].

@entity1 @entity101 @entity35 @entity7196 @entity1184 @entity1808 @entity4346 @entity1811 @entity472 @entity11154
Chronic mechanical stress of the heart by @entity101 is a primary cause of @entity4346 . 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 ( @entity1811 ) is increased resulting in elevated cardiac @entity1808 formation. This has been demonstrated in stretched cardiac myocytes in vitro as well as in animal models of pressure overload @entity1184 ( @entity7196 and spontaneously @entity101 @entity35 ) and in @entity1 pressure overload @entity1184 ( @entity472 ). Functional consequences of elevated @entity1808 levels may be vasoconstriction of the coronary vasculature and a deterioration of diastolic function of the hypertrophied heart. Local formation of @entity1808 may also have proliferative effects on cardiac myocytes and connective tissue cells. @entity1808 may, thus, be an important factor causing development and progression of @entity4346 by itself. Blockade of the renin-angiotensin system has been found to be an effective treatment of @entity101 , probably better than any other antihypertensive medication. Regression of @entity4346 has been achieved by blockade of the @entity1808 pathway either by administration of an angiotensin-converting enzyme inhibitor or an @entity11154 blocker. The animal model of @entity7196 has been used to show beneficial effects of blockade of the renin-angiotensin system on @entity1184 and survival. In this @entity35 model regression of @entity4346 by @entity1811 -inhibition or @entity11154 blockade could be demonstrated by serial echocardiographic analyses while afterload of the left ventricle was still elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
