AJP - Heart and Circulatory Physiology, Vol 252, Issue 4 692-H696, Copyright © 1987 by American Physiological Society
Atrial natriuretic factor secretion in dogs with experimental high-output heart failure
D. Villarreal, R. H. Freeman, J. O. Davis, K. M. Verburg and R. C. Vari
The temporal changes in the plasma concentration of immunoreactive atrial
natriuretic factor (iANF) were studied in six conscious dogs with an
arteriovenous (AV) fistula, a model of chronic high-output heart failure.
Following the creation of the AV fistula, the dogs retained sodium avidly
for 5 days, and plasma renin activity, plasma aldosterone concentration,
and right atrial pressure increased significantly from controls. During
this initial stage, iANF increased only modestly. From day 6 to 14, the
dogs increased their daily sodium excretion and approached sodium balance.
This natriuretic response was associated with a significant rise in iANF,
with the return of renin and aldosterone levels to base line, and with a
progressive significant elevation in right atrial pressure. Thus, in dogs
with an AV fistula and cardiac volume overload, chronic increases in atrial
pressure appear to be a sustained stimulus for the release of ANF. It is
suggested that following the initial period of sodium retention in this
experimental mental model of heart failure, chronic endocrine adjustments
for the reestablishment of sodium balance involve an increase in ANF which
subsequently can exert a tonic inhibitory action on the renin-aldosterone
axis. It is concluded that the ANF endocrine system might function as an
effective chronic compensatory mechanism to help promote sodium and water
excretion in dogs with an AV fistula through the suppression of the
renin-aldosterone system and possibly through its direct renal actions.
