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We studied the role of renal papillae in the mechanism of increased sodium excretion during acute increase in mean arterial pressure (MAP). Sodium excretion increased dramatically in normal rats after acute increase in MAP by epinephrine (E) infusion (0.4 micrograms/min/100g). Glomerular filtration rate (GFR), renal blood flow (RBF), and papillary plasma flow (PPF) remained unchanged after the E administration. To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide. Urinary sodium and fractional sodium excretions were 2.00 +/- 0.34 microEq/min and 2.37 +/- 0.53% (n = 7), respectively, in papillary necrosis rats infused with saline. Administration of E to papillary necrosis rats, however, failed to increase both urinary sodium (2.89 +/- 0.61 microEq/min) and fractional sodium (FENa, 2.82 +/- 0.63%, n = 6) excretions despite a marked increase in MAP (129 vs 150 mm Hg, p less than 0.01). The RBF increased slightly after E infusion (4.42 vs 3.24 ml/min/100 g, p less than 0.05), but the GFR was not different between the control (0.39 +/- 0.05 ml/min/100g, n = 7) and the E-treated rats (0.43 +/- 0.06, n = 6). Failure to increase sodium excretion during acute increase in MAP was not due to the decreased GFR, since control rats with bilateral partial nephrectomy were able to increase sodium excretion from 1.92 +/- 0.33 to 7.76 +/- 1.63 microEq/min (p less than 0.01) after E infusion. These findings, therefore, suggest that renal papillae play a major role in the mechanism of natriuresis during acute increase in MAP.

Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat.