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AJP - Heart and Circulatory Physiology, Vol 270, Issue 2 594-H602, Copyright © 1996 by American Physiological Society
ARTICLES |
M. T. Rademaker, C. J. Charles, E. A. Espiner, C. M. Frampton, M. G. Nicholls and A. M. Richards
Department of Medicine, Christchurch School of Medicine, New Zealand.
The responses of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were investigated in six conscious sheep paced at 120, 155, 190, and 225 beats/min for 1.5 h at each rate and at 180, 225, and 180 beats/min for 4 days at each rate. Increased pacing reduced arterial pressure, cardiac output, and urine and Na excretion and increased left atrial pressure and plasma ANP, BNP, and C-type natriuretic peptide, with delayed activation of the renin-angiotensin system (RAS). Acute pacing increased plasma ANP and BNP levels 8.6- and 3.6-fold, respectively (both P < 0.001), whereas chronic pacing increased ANP and BNP 7.8- and 9-fold, respectively (both P < 0.001). Thus the ANP-to-BNP ratio increased during acute pacing (P < 0.001) and decreased proportionately during chronic pacing (P < 0.05). Reduction in pacing improved hemodynamic status, reduced natriuretic peptides (BNP less than ANP), normalized the RAS, and induced diuresis and natriuresis. In conclusion, BNP is less responsive than ANP to acute changes in intracardiac pressure but is proportionately more responsive to chronic hemodynamic changes such as occur in congestive heart failure.
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