Left ventricular hypertrophy (LVH) is an independent marker of mortality in hypertension. Although the
mechanisms contributing to LVH are complex, inflammation and oxidative stress may favor its development. We analyzed
the association of the phagocytic NADPH oxidase–mediated superoxide anion release and LVH in patients with essential
hypertension and the role of cardiotrophin-1 (CT-1) and interleukin-6 (IL-6), cytokines implicated in cardiac growth.
Blood pressure, echocardiography data, and serum CT-1 and IL-6 levels were obtained in 140 subjects: 18 normotensives
without LVH, 42 hypertensives without LVH, and 80 hypertensives with LVH. The NADPH oxidase–dependent superoxide
production was assessed by chemiluminescence in peripheral blood mononuclear cells. Peripheral blood mononuclear
cells were stimulated with CT-1 in vitro. Superoxide anion production by peripheral blood mononuclear cells associated
with LVH and correlated with the left ventricular mass index. Serum CT-1 and IL-6 levels, which associated with the
left ventricular mass index, correlated with superoxide production. Serum CT-1 and IL-6 levels were correlated. CT-1
stimulated NADPH oxidase superoxide production in peripheral blood mononuclear cells, which resulted in an increased
release of IL-6. Our results show that superoxide anion production by the phagocytic NADPH oxidase associates with
hypertensive heart disease, being significantly enhanced in hypertensive patients with LVH. This may be attributable to
the activation of the NADPH oxidase by CT-1 and the subsequent release of IL-6. The phagocytic NADPH oxidase may be a therapeutic target in hypertensive heart diseas
