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Left ventricular hypertrophy (LVH) and fibrosis have received special attention as possible therapeutic targets in preventing cardiovascular complications of hypertension. Suppression of neurohormonal factors that predispose to target organ damage, in addition to blood pressure (BP) reduction, seems to be of importance in modulating cardiac remodeling and fibrosis in hypertensive heart disease. In the normal heart, the effects of endogenous hypertrophic/profibrotic factors, including angiotensin II (Ang II), aldosterone, and inflammatory cytokines, such as transforming growth factor-β, growth factors, and catecholamines, are balanced by the action of growth-inhibiting/antifibrotic factors, including NO, natriuretic peptides, and bradykinin.Previous studies have shown that atrial natriuretic peptide (ANP) modulates cardiac hypertrophy and fibrosis in response to a variety of hemodynamic stresses.1–3 In the setting of hypertension or in the absence of the counterregulatory effects of ANP signaling, as in the ANP null ( Nppa −/−) or heterozygous ( Nppa +/−) mouse or the mouse lacking natriuretic peptide type A receptors ( Npr −/−), the unopposed profibrotic/hypertrophic factors predominate, and …

Is There a New Treatment for Hypertensive Disease in the Horizon?