ANGIOTENSIN AND ANP SECRETION DURING CHRONICALLY CONTROLLED INCREMENTS IN ATRIAL PRESSURE

The primary objective of this study was to determine whether angiotens in II (ANG II) has direct effects on the atrium to chronically stimula te the secretion of atrial natriuretic peptide (ANP) by actions that a re independent of its vasoconstrictor and fluid-retaining effects that increase ANP secretion indirectly by raising atrial pressure. In five dogs, right atrial pressure (RAP) was controlled at similar to 5.5 mm Hg above control levels for 8 days by employing an externally adjustab le occluder around the pulmonary artery and a servo-control system, an d plasma levels of ANG II were fixed at either normal (days 1-3 and 7- 8) or high (days 4-6) physiological concentrations by chronic infusion of captopril + ANG II, When plasma ANG II was maintained at normal le vels during servo-control of RAP, plasma ANP concentration increased f ive- to sixfold and sodium balance was achieved at a reduced arterial pressure (-14 mmHg). In contrast, despite increased plasma levels of A NP, the high rate of ANG II infusion produced marked sodium retention during the initial 24 h; however, the antinatriuresis was not sustaine d because the servo-control system partially deflated the pulmonary ar tery occluder to prevent fluid-induced increments in RAP. Moreover, in the absence of a change in RAP, high plasma levels of ANG II did not influence plasma ANP concentration. These findings indicate that the p lasma levels of ANP achieved in heart failure increase renal excretory capability and allow fluid balance to be achieved at a substantial fa ll in mean arterial pressure as long as there is minimal involvement o f the renin-angiotensin system. Furthermore, in contrast to pronounced renal actions, high plasma levels of ANG II do not chronically increa se ANP secretion under conditions of elevated atrial pressure by direc tly stimulating atrial ANG II receptors.