AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 4 607-R610, Copyright © 1988 by American Physiological Society
Role of atrial pressure and rate in release of atrial natriuretic peptide
K. P. Walsh, T. D. Williams, C. Spiteri, E. Pitts, S. L. Lightman and R. Sutton
Department of Cardiology, Westminster Hospital, London, United Kingdom.
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.
