The Effect of Renal Perfusion Pressure on the Net Transport of Sodium Out of Distal Tubular Urine As Studied with the Stop-Flow Technique*

Abstract

After a 55-minute perfusion of isolated rat kidneys at 170 mm Hg, the tubular cells in the distal part of the nephron have a relative limited ability to effect a net transport of sodium out of the distal tubular urine in a stop-flow situation. In two series of experiments utilizing this high perfusion pressure, the lowest concentration of sodium in the stop-flow studies averaged 31 mEq per 1 and 25 mEq per 1, respectively. Conversely, after a 5-minute perfusion at 100 mm Hg, the distal tubular cells have a relatively enhanced ability to effect a net transport of sodium out of the distal urine. In a series of experiments utilizing this lower perfusion pressure, the lowest concentration of sodium in the stop-flow studies averaged 14 mEq per 1. In a subsequent comparison using a different stop-flow method, the high perfusion pressure resulted in an average minimal sodium concentration of 13.7 mEq per kg, whereas the low perfusion pressure produced an average minimal sodium concentration of 7.9 mEq per kg. This difference in net transport of sodium seems related more to the perfusion pressure than to the rate of blood or urine flow. Renal hemodynamics and the rate of flow in the renal tubules during the stop period cannot account for the difference. The difference in net sodium transport does not depend upon a changing rate of aldosterone secretion or upon neurogenic reflexes from the central nervous system. Apparently, changing the distention of the renal arterial bed by altering perfusion pressure somehow influences the ability of distal tubular cells to effect a net transport of sodium, underdistention increasing transport and overdistention decreasing it. The authors speculate that the varying levels of perfusion pressure are sensed by the granular juxtaglomerular cells, acting as stretch receptors. The juxtaglomerular apparatus (granular cells plus macula densa cells) then appropriately responds by changing its rate of secretion. The concentration of these secretory substances in the fluids of the kidney subsequently regulates the net transport of sodium in the distal convoluted tubule and collecting duct, acting in concert with the tissue levels of aldosterone. This mechanism is probably active in various sodium-retaining situation associated with underdistention of the arterial tree. It may also partially explain the phenomenon of the Howard test.