Angiotensin blocking drugs and the heart beyond 2000.

Cardiac hypertrophy can be caused in different ways, and the effect of hypertrophy on prognosis depends on whether it is concentric or eccentric in nature. It is simplistic to ascribe hypertrophy purely to workload, and it is a complex interaction between workload, wall stress, and the local and humoral environment. In rats, acute elevation of BP occurring during the rats' sleep cycle causes cardiac hypertrophy, and reduction of BP in hypertensive rats during the sleep cycle causes reversal of left ventricular hypertrophy. This may be due to secretion of growth hormone and renin during sleep. Experimental evidence indicates that angiotensin II possibly formed and acting locally may be implicated in the genesis of cardiac hypertrophy; however, angiotensin II by itself causes relatively minor hypertrophy, but this becomes intensified if there is a high sodium intake and a high angiotensin II level. Blockade of the angiotensin system with angiotensin-converting enzyme inhibitors causes reversal of cardiac hypertrophy and similar results are achieved with AT1 receptor blocking drugs, suggesting that bradykinin may be of relatively minor importance. Clinically, the AT1 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.