AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 2 422-R426, Copyright © 1989 by American Physiological Society
Natriuretic response to hypervolemia is absent in rats with papillary necrosis
R. Keeler and N. Wilson
Department of Physiology, University of British Columbia, Vancouver, Canada.
The renal responses to acute expansion of the blood volume (20%), acute
saline loading (5% body wt), or administration of atrial natriuretic
peptide (ANP) were investigated in rats 7-10 days after inducing
experimental renal papillary necrosis by the injection of bromoethylamine
hydrobromide. In normal rats, urinary Na output (UNaV) increased from 1 +/-
0.4 to 16.6 +/- 1.7 mumol/min. In rats with papillary necrosis, UNaV only
increased from 1.1 +/- 0.2 to 2.5 +/- 0.5 mumol/min. In contrast, the
natriuretic responses to saline loading in normal rats (from 1.7 +/- 0.2 to
21.6 +/- 2.4 mumol/min) and to the infusion of ANP (from 0.8 +/- 0.1 to 7.6
+/- 0.8 mumol/min) were not significantly attenuated in rats with papillary
necrosis. The absence of a natriuretic response to hypervolemia in rats
with papillary necrosis was not a result of failure to secrete ANP, because
plasma levels of immunoreactive ANP increased three- to four-fold in rats
with papillary necrosis and in untreated rats. It is concluded that the
mechanisms mediating the natriuretic and diuretic responses to acute
expansion of the blood volume mainly involve alterations in inner medullary
function. In contrast, natriuretic responses to saline loading and
pharmacological doses of ANP are apparently mediated by more superficial
cortical nephrons.
