The potential role of nitric oxide in the hypertrophic growth of the left ventricle

Left ventricular hypertrophy (LVH) is the result of interaction between a c hronic hemodynamic over load and non-hemodynamic factors. There ale several lilies of evidence presented in this work suggesting that nitric oxide (NO ) may participate in the hypertrophic growth of the myocardium, First, endo thelial NO production was shown to be decreased in several types of hemodyn amically overloaded circulation both in animals and humans. Second. compoun ds stimulating NO production were able to diminish the extent or modify the nature of LVH in sonic models of myocardial hypertrophic growth. Third, ar terial hypertension can be induced by inhibition of nitric oxide synthase a ctivity, This NO-deficient hypertension is associated with the development of concentric LVH, myocardial fibrosis and protein remodeling of the left v entricle. The mechanism of LVH development in NO-deficient hypertension is complex and involves decreased NO production and increased activation of th e renin-angiotensin-aldosterone system. Cardiovascular protection I,ia ACE inhibition in NO-deficient hypertension may be induced by mechanisms not in volving all improvement of NO production. Tn conclusion, the hypertrophic g rowth of the LV appears to be the result of interaction of vasoconstrictive and growth stimulating effects of angiotensin II on the one hand and of va sodilating and antiproliferative effects of nitric oxide on the other.