FIGURE 20.

Proposed effects of 20-hydroxyeicosatetraenoic acid (20-HETE) signaling on transport in the Dahl rat. A: the 20-HETE physiology in R. B: the ultimate cause for decreased 20-HETE levels in S remains unknown. However, the reported decreased in cytochrome P-450 A2 (CYP450A2) protein expression and defective angiotensin II type 2 receptor (AT₂R) signaling are expected to reduce the formation of 20-HETE. Concomitantly, excess superoxide (${\mathrm{O}}_2^{-}$) may further lower 20-HETE bioavailability. Together, these effects could increase thick ascending limb NaCl reabsorption on S, by lack of inhibitory signals on Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2), Na⁺/H⁺ exchanger type 3 (NHE3), and renal outer medullary K⁺ channel (ROMK).