Atrial stretch, not pressure, is the principal determinant controlling the acute release of atrial natriuretic factor

The current studies were designed to investigate the mechanisms in the intact anesthetized dog that control the release of atrial natriuretic factor (ANF). In vitro, mechanical stretch of atrial tissue produces an increased release of ANF. In vivo, changes in atrial pressure correlate positively with circulating ANF levels. The present investigations used 6 open-chest anesthetized dogs to evaluate the role of atrial pressure versus atrial stretch, the latter determined by atrial transmural pressure, in the release of ANF. In a paired design, animals underwent cardiac tamponade followed by constriction of the aorta and pulmonary artery. Tamponade produces a balanced increase in intra-atrial and pericardial pressures. Thus, despite an elevated atrial pressure, there is no increase in transmural pressure producing atrial stretch. Great artery constriction increases intra-atrial but not pericardial pressure, resulting in an increase in atrial transmural pressure and atrial stretch. Cardiac tamponade increased right atrial pressure (0.8 ± 0.3 to 7.6 ± 0.6 mm Hg, p < 0.001) and pulmonary capillary wedge pressure (3.7 ± 0.6 to 8.8 ± 0.6 mm Hg, p < 0.001). Constriction of the aorta and pulmonary artery also increased right atrial pressure (1.5 ± 0.8 to 6.3 ± 0.8 mm Hg, p < 0.05) and pulmonary capillary wedge pressure (4.6 ± 0.3 to 7.8 ± 1.0 mm Hg, p < 0.05). Atrial transmural pressure increased only during great artery constriction. ANF release increased only during great artery constriction from 73 ± 15 to 255 ± 53 pg/ml, p < 0.05, while there was no change in circulating ANF during tamponade, 51 ± 3 to 52 ± 11 pg/ml. These studies demonstrate that an increase in atrial transmural pressure with associated atrial stretch, not increased intra-atrial pressure, acts as the principal mediator controlling the acute release of ANF.