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NHE3 becomes phosphorylated during acute hypertension

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 Na+ transporter activity along the nephron. We aimed to test the hypothesis that the phosphorylation status of proximal tubule NHE3, medullary NKCC2 and renal AMP kinase is altered during acute hypertension. Background: Dopamine increases NHE3‐P at Ser 552 (Kocinsky, 2005); NKCC2‐P at Thr212/Thr217 is associated with translocation to the plasma membrane (Giménez, 2003); AMPK‐P (Thr172) decreases ENaC activity (Hallows, 2005). BP was increased for 15 min in anesthetized rats by vascular constriction (vs. sham). Kidneys were excised, homogenized with phosphatase and protease inhibitors, and abundance of total and phosphorylated forms of NHE3, NKCC2 and AMPK quantitated with specific antibodies. NHE3‐P at Ser552 doubled in abundance during hypertension. No significant changes in NKCC2‐P or AMPK‐P abundance were evident. Density distribution patterns and lipid domain properties of total and –P forms of NHE3 were identical at baseline BP and after high BP. We conclude that acute hypertension provokes a rapid phosphorylation of NHE3 at ser552 that may participate in the decrease in proximal tubule sodium reabsorption, by provoking changes in NHE3 distribution, activity or protein association. DK34316, NIH Step‐Up (EL).