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INTERNALIZATION OF DCT Na‐Cl‐CO‐TRANSPORTER (NCC) DURING PRESSURE DIURESIS‐NATRIURESIS

When blood pressure (BP) is elevated above baseline, a pressure natriuresis response ensues which is critical to volume and blood pressure homeostasis. The response involves a decrease in salt and volume reabsorption from proximal tubule and a load dependent increase in salt reabsorption in loop of Henle. The role of distal nephron is less clear. Distal convoluted tubule Na+‐Cl− cotransporter (NCC) is regulated by trafficking between apical plasma membrane (APM) and sub‐apical cytoplasmic vesicles (SCV). We aimed to determine whether NCC trafficking contributes to pressure natriuresis (increase APM NCC) or compensates for increased volume flow to the DCT (decrease APM NCC). BP was raised 50 mmHg (hiBP) for 30 min in rats by arterial constriction. Kidneys were excised and NCC subcellular distribution analyzed on sorbitol density gradients by immunoblot or kidneys were perfusion fixed and NCC analyzed by immuno‐electron microscopy. After 30 min hiBP urine output increased 11‐fold. By density gradient, 20% of the total NCC redistributed from low density APM to higher density fractions (p<0.05). By quantitative immuno‐EM pool size of APM NCC decreased 13% with a corresponding increase in the SCV pool (p<0.05). In summary, the results provide evidence for an acute decrease in APM NCC during hypertension that likely contributes to pressure diuresis‐natriuresis. HL085388, DK34316, Danish NRF.