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.