Cardiac tissue-generated angiotensin II plays a major role in volume overload-induced cardiac hypertrophy, but its role in pressure overload and post-myocardial infarction remodeling remains unclear.
In the past decade evidence has accumulated for local tissue renin-angiotensin systems and for direct trophic effects of angiotensin II. In the present update we review new evidence for the independent generation of cardiac angiotensin II and its relevance for cardiac pathophysiology. A major role of angiotensin II generated by cardiac tissue has become apparent for the development of volume overload-induced cardiac hypertrophy. In contrast, evidence that cardiac pressure overload is associated with increased generation of angiotensin II by cardiac tissue is missing, and a role for angiotensin II produced by cardiac tissue in pressure overload-induced cardiac hypertrophy remains to be addressed. Similarly, although evidence has accumulated for increased gene expression and production of components of the renin-angiotensin system in the area adjacent to a myocardial infarction, data on changes in cardiac angiotensin II in infarcted or remnant myocardium are very limited. Without these, one can not assess whether blockade of angiotensin II generated by cardiac tissue contributes to the beneficial effects of blockers of the renin-angiotensin system on cardiac remodeling postmyocardial infarction.
Ruzicka et al. (Tue,) conducted a review in Cardiac hypertrophy and myocardial infarction. Cardiac tissue-generated angiotensin II was evaluated. Cardiac tissue-generated angiotensin II plays a major role in volume overload-induced cardiac hypertrophy, but its role in pressure overload and post-myocardial infarction remodeling remains unclear.