Angiotensin blocking drugs and the heart beyond 2000

Cardiac hypertrophy can be caused in different ways, and the effect of hype rtrophy on prognosis depends on whether it is concentric or eccentric in na ture. It is simplistic to ascribe hypertrophy purely to workload, and it is a complex interaction between workload, wall stress, and the local and hum oral environment. In rats, acute elevation of BP occurring during the rats' sleep cycle causes cardiac hypertrophy, and reduction of BP in hypertensiv e rats during the sleep cycle causes reversal of left ventricular hypertrop hy. This may be due to secretion of growth hormone and renin during sleep. Experimental evidence indicates that angiotensin II possibly formed and act ing locally may be implicated in the genesis of cardiac hypertrophy; howeve r, angiotensin II by itself causes relatively minor hypertrophy, but this b ecomes intensified if there is a high sodium intake and a high angiotensin II level. Blockade of the angiotensin system with angiotensin-converting en zyme inhibitors causes reversal of cardiac hypertrophy and similar results are achieved with AT, receptor blocking drugs, suggesting that bradykinin m ay be of relatively minor importance. Clinically, the AT, receptor blocking drugs have few side effects and appear to have similar beneficial effects to angiotensin-converting enzyme inhibitors, making them suitable to treat many people with hypertension.