Angiotensin and the remodelling of the myocardium.

From a morphologic standpoint, the myocardium has three compartments: cardiac myocytes; intramyocardial coronary arteries with a microcirculation; and an interstitium composed largely of fibrillar collagen. As long as intercompartmental equilibrium exists, myocardial mechanics and energetics and myocyte viability will each be preserved. 2. The hypertrophic process seen with left ventricular pressure overload secondary to renovascular hypertension alters this equilibrium because of the adverse remodelling of intramural coronary arteries and fibrillar collagen. The pathogenetic mechanism(s) responsible for the observed myocardial fibrosis, having reactive and reparative components, remains to be elucidated. 3. Attractive circumstantial evidence, however, has been obtained to incriminate circulating angiotensin II in this process. Five lines of evidence favouring the role of angiotensin II in promoting the reactive perivascular and interstitial fibrosis and the reparative fibrosis are presented, including the potential cardioprotective effects of angiotensin converting enzyme inhibitors.