Tubular Sodium Reabsorption and the Regulation of Renal Hemodynamics. The Effect of Hypertonic Saline Infusion on Renal Vascular Resistance

The hemodynamic response following saline loading was found to differ from that induced by the saluretic agent, chlorothiazide, which causes vasoconstriction. When hypertonic NaCl was infused into the renal artery until a profuse sodium diuresis was obtained, and the infusion then interrupted, C_Na/C_In remained elevated for 60–80 min. During this period the renal vascular resistance did not change significantly and the glomerular filtration rate tended to rise as compared with the control periods. This is contrary to what has previouly been found during chlorothiazide administration, where renal vascular resistance was significantly correlated with C_Na/C_In. A hypertonic saline load blocks Na reabsorption in the proximal tubules, chlorothiazide mainly in the distal tubules. It was therefore concluded that it is a reduction of movement of Na into the distal tubule cells, specifically the macula densa, rather than the increased Na concentration of the distal tubular fluid that is responsible for the vasoconstrictive effect of chlorothiazide.