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AJP - Renal Physiology, Vol 253, Issue 6 1129-F1135, Copyright © 1987 by American Physiological Society
ARTICLES |
R. W. Barbee and N. C. Trippodo
Division of Research, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
To explore the role of atrial natriuretic factor (ANF) in acute volume-expansion natriuresis, right atrial pressure (RAP), mean arterial pressure (MAP), rate of urinary sodium excretion (UNaV), and plasma immunoreactive ANF (IR-ANF) were measured in anesthetized, open-chest rats. All groups received 33% blood volume expansion with whole blood in 15 min. RAP was not allowed to increase in one group by using a caval snare. MAP was controlled in a second group with the use of an aortic snare. A third group (RAP-controlled ANF) with control of RAP received rat ANF (99-126) at doses designed to mimic the IR-ANF measured in the MAP-controlled rats. IR-ANF was similar 5 min after blood infusion in rats exhibiting increased RAP (490 +/- 111 pg/ml) and in those without increased RAP but receiving ANF infusion (447 +/- 44 pg/ml); this was also true at 45 min after blood infusion (232 +/- 44 vs. 263 +/- 27 pg/ml). IR-ANF in rats with constant RAP (without ANF infusion) remained low throughout the experiment (61 +/- 10 and 74 +/- 10 pg/ml). UNaV increased only in the MAP-controlled and ANF-infused groups, but peak responses occurred 15-30 min after the onset of volume expansion in the former, and 60-75 min in the latter. Thus, factors other than ANF mostly accounted for the immediate natriuresis after volume expansion, whereas ANF predominated after a delayed period. The results suggest that increased plasma ANF accounted for at least 34% of the observed natriuretic response to acute volume expansion in anesthetized rats.
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