The renin-angiotensin system and cardiac hypertrophy.

The heart develops left ventricular hypertrophy (LVH) in response to increased afterload in order to compensate for its wall stress and to maintain normal cardiac function.' Although the development of cardiac hypertrophy is itself an adaptive phenomenon, it is an important cause of increased morbidity and mortality.2 Thus cardiac hypertrophy has recently attracted attention as an important risk factor influencing the prognosis of patients with hypertension. Recently, much data have been accumulated with regard to the molecular mechanisms of cardiac hypertrophy. Recent advances include demonstration of the existence of the local renin-angiotensin system in the heart3 and involvement of angiotensin II in the formation of cardiac hypertrophy.4 In this paper we examine signal transduction pathways in cardiac hypertrophy that are induced by stress, and how the relation between mechanical stress and the local reninangiotensin system affects cardiac hypertrophy.