AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 1 86-R90, Copyright © 1989 by American Physiological Society
Proximal tubule response in aldosterone escape
J. M. Gonzalez-Campoy, J. Kachelski, J. C. Burnett Jr, J. C. Romero, J. P. Granger and F. G. Knox
Department of Physiology and Biophysics, Mayo Medical School, Rochester, Minnesota 55905.
The response of the proximal tubule to chronic aldosterone administration
(15 micrograms.kg-1.day-1) was evaluated in eight conscious female mongrel
dogs. Temporal profiles between hemodynamic and hormonal changes and the
fractional excretions of sodium and lithium were established. Aldosterone
infusion resulted in a significant decrease in urinary sodium excretion
from 9.2 +/- 1.3 to 5.8 +/- 0.9 meq/h after 1 day, returning to normal by
the 5th day. These changes in urinary sodium excretion were associated with
significant elevations of the mean arterial pressure (MAP) from 105 +/- 5
to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF)
from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Plasma
renin activity (PRA), on the other hand, was depressed by aldosterone,
falling below the level of detectability. The fractional excretion of
lithium increased significantly by day 2 of aldosterone infusion (from 29
+/- 3 to 44 +/- 6%), reflecting the proximal tubular response to the above
changes. We conclude that the proximal tubule responds to increases in MAP
and ANF and decreases in PRA during aldosterone infusion by decreasing
sodium reabsorption. Subsequent nephron segments must also respond to the
volume expansion produced by aldosterone, since the sustained proximal
tubule natriuretic response is insufficient to explain all of escape.
