Na,K‐ATPase in the Plasma Membrane of the Rat Proximal Tubule is Increased by An Acute Reduction in Renal Perfusion Pressure

Abstract

Increases in blood pressure inhibit sodium reabsorption in proximal tubule (Zhang, Y. et al., Am. J. Physiol. 274:C1090, 1998). Conversely, an acute decrease in renal perfusion pressure should stimulate sodium reabsorption. To test this hypothesis we placed a constricting ligature around the aorta between the renal arteries, and monitored perfusion pressure to kidneys above and below the constriction in anesthetized male Sprague-Dawley rats. Perfusion pressure to the left kidney was reduced to 69 ± 1mm Hg by tightening the ligature. Right renal perfusion pressure was 107 ± 4 mm Hg. Pressures were maintained constant for 10 min, after which the kidneys were flushed, excised, and the cortex dissected, minced, and sieved. The cell mixture was centrifuged and the proteins in the pellet biotinylated at pH 9.0. Membrane proteins were extracted, and biotinylated plasma membrane proteins isolated with immobilized streptavidin. Based on western blotting and densitometry, there was a 75% ± 35% (P< 0.03) increase in arbitrary units in the immunoblot signal from the alpha-subunit of Na, K-ATPase from kidneys subjected to the lower perfusion pressure compared to normal pressure. There was no difference observed in sham constricted controls (n=4). Since increased amounts of Na,K-ATPase in the plasma membrane should promote sodium reabsorption, our data suggest that acutely reduced renal perfusion results in increased proximal sodium reabsorption mediated by enhanced incorporation of Na,K-ATPase into the proximal plasma membrane. Supported by DK60752-01A1.