ANP expression in the hypertensive heart.

Atrial natriuretic peptide (ANP), the principal member of the natriuretic factor family of peptides, primarily a product of the atria in the adult heart, is also expressed in the fetal ventricles. A minority of ventricular impulse-conducting cells and myocytes exposed to extreme tension retain the capacity to produce ANP in the adult. The number and distribution of ANP-expressing cells increases dramatically when the ventricle is pressure loaded and hypertrophied, as in the case of chronic hypertension. Coregulation of hypertrophy and ANP expression has established this peptide as a marker of myocardial hypertrophy and of the activation of the fetal gene program, typical of this condition. However, a coordinated reduction of hypertension and ANP expression while hypertrophy persists indicates that the hemodynamic state overrules hypertrophy in controlling ANP expression in hypertensive rat hearts. Under these circumstances, reduced activity of the cardiac-restricted transcription factor GATA-4 (a regulator of both hypertrophy and ANP expression) correlated with ANP downregulation but not with hypertrophy, which remained unchanged. Therefore, maintenance of cardiac hypertrophy in essential hypertension may not be dependent solely on GATA activity: it seems that additional factors may be involved. It is suggested that cell size and ANP production are autonomous features of the myocyte in the hypertensive heart and, although governed by similar mechanisms, the two features may be manifested independently.