To investigate whether atrial natriuretic peptide (ANP) release during paroxysmal tachycardia is due to increased atrial rate or increased atrial pressure, plasma ANP concentrations were measured during atrial pacing at increasing rates in six alpha-chloralose-anesthetized dogs whose atrial pressures were maintained artificially low by balloon occlusion of the inferior vena cava (IVC). These ANP concentrations were compared with those seen during identical increasing atrial rates in the same dogs without IVC occlusion. During incremental pacing without IVC occlusion, pulmonary wedge pressure (PWP; mean +/- SE) rose progressively from 5.3 +/- 1.6 at 200 to 20.2 +/- 2.3 mmHg at 350 beats/min (P less than 0.01), and right atrial pressure (RAP) rose progressively from 2.5 +/- 0.9 at 200 to 6.7 +/- 2.1 mmHg at 350 beats/min (P less than 0.05). At the same time, arterial and coronary sinus ANP concentrations rose from 116 +/- 55 and 339 +/- 91 to 1,126 +/- 226 and 1,960 +/- 456 pmol/l, respectively (P less than 0.01). In contrast, incremental pacing with IVC occlusion produced no significant increase in PWP and RAP. Arterial and coronary sinus ANP concentrations during IVC occlusion were, respectively, 208 +/- 126 and 388 +/- 159 at 200 and 261 +/- 83 and 345 +/- 80 pmol/l at 350 beats/min (NS). This study demonstrates that the release of ANP during tachycardia is primarily dependent on increased atrial pressure and not atrial rate.
Secretion of human atrial natriuretic peptide in response to atrial pacing and its function in patients with ventricular septal defect.