Role of pendrin in iodide balance: going with the flow

Abstract

Pendrin is expressed in the apical regions of B and non‐A, non‐B intercalated cells, where it mediates apical Cl−/HCO3− exchange. Pendrin is a robust I− transporter. So, we asked if I− restriction modulates pendrin abundance and if I− balance is altered in pendrin null mice. Pendrin abundance was evaluated with immunoblots, immunohistochemistry and immunogold cytochemistry with morphometric analysis. While pendrin abundance was unchanged when dietary I− intake was varied, I− balance differed in pendrin null and in wild type mice. Serum I− was lower, while I− excretion was higher in pendrin null relative to wild type mice, consistent with a role of pendrin in renal I− absorption. Increased H2O intake enhanced differences between wild type and pendrin null mice in I− balance, suggesting that H2O intake modulates pendrin abundance. Increasing water intake raised B cell apical plasma membrane pendrin abundance. Water intake did not modulate pendrin abundance by changing circulating renin or aldosterone concentration or by changing serum osmolality or circulating vasopressin. Moreover, in models of vasopressin escape serum Cl− was much lower in pendrin null than in wild type mice. We conclude that water intake modulates pendrin abundance. As water intake rises, pendrin becomes increasingly critical in the maintenance of Cl− and I− balance.