AJP - Renal Physiology, Vol 253, Issue 5 880-F883, Copyright © 1987 by American Physiological Society
Possible modulatory role of angiotensin II on atrial peptide-induced natriuresis
F. J. Salazar, J. P. Granger, M. J. Fiksen-Olsen, M. D. Bentley and J. C. Romero
Department of Physiology, School of Medicine of Murcia, Spain.
Studies showing that atrial natriuretic peptides (ANP) induce a suppression
of the renin-angiotensin system suggest that there might be a modulatory
influence of angiotensin II (ANG II) on the natriuretic effect of the ANP
system. To evaluate this possibility we assessed, in anesthetized dogs, the
net increments in fractional excretion of sodium (FENa) and lithium (FELi)
produced by ANP and by the inhibition of ANG II formation with captopril.
These agents were infused at separate time periods into the renal artery at
a maximal level that has been shown not to alter glomerular filtration rate
(GFR). ANP caused an increment in FENa of 4.0 +/- 0.2, whereas captopril
caused a much smaller increase of 0.2 +/- 0.04, indicating that most of the
natriuretic effect of ANP is unlikely to be solely accounted for by
inhibition of ANG II. The administration of both ANP and captopril produced
increases in the FELi used as a marker for proximal tubular reabsorption.
An infusion of ANG II superimposed on the infusion of captopril reduced the
FENa from 1.5 +/- 0.3 to 0.8 +/- 0.1. Under these conditions the
administration of ANP produced an increment of 2.7 +/- 0.4 in the FENa.
This increase in FENa is 32.5% less than the net increase obtained when ANP
was given in the absence of ANG II, whereas under these conditions FELi
remained statistically unchanged. These results suggest that the modulatory
activity of ANG II on the natriuretic affect of ANP could be negligible
under normal conditions.
