Natriuretic response to hypervolemia is absent in rats with papillary necrosis

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.