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AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 1 247-R254, Copyright © 1991 by American Physiological Society
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L. M. Harrison-Bernard, R. C. Vari, W. H. Holleman, N. C. Trippodo and R. W. Barbee
Department of Physiology, Tulane University School of Medicine, New Orleans 70112.
The present study was designed to examine acute (2 h) and chronic (5 day) effects of pathophysiological elevations of plasma atrial natriuretic factor (ANF) in conscious normotensive rats. Acute infusion of ANF (100 ng.kg-1.min-1; n = 15) resulted in a decrease in mean arterial pressure (MAP) of 5 +/- 3 mmHg, which was associated with a 23 +/- 4% decrease in cardiac output (CO) and a 27 +/- 6% increase in total peripheral resistance (TPR). Hematocrit increased from 41.9 +/- 0.7 to 46.0 +/- 0.6%, which is suggestive of vascular volume contraction. Chronic infusion of ANF (n = 9) produced a significant fall in MAP from a control value of 114 +/- 2 to 100 +/- 3 and 99 +/- 2 mmHg on days 1 and 5, respectively. CO decreased significantly (27 +/- 2%) and TPR increased (21 +/- 5%) on day 1; neither variable was significantly different from control on day 5. Plasma immunoreactive ANF levels were significantly elevated during acute (791 +/- 76 pg/ml) and chronic (626 +/- 202 pg/ml) ANF infusion compared with control values of approximately 100 pg/ml. The results indicate that elevations in plasma ANF within the pathophysiological range can significantly alter systemic hemodynamics, initially mediated by a decrease in CO. Autoregulatory phenomena may counteract these hemodynamic effects, returning CO to control levels and reducing TPR when the elevations in plasma ANF are chronically sustained.
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