Figure 1.

(A) and (B) Arginine vasopressin (AVP)‐mediated intraglomerular hypertension (HTN), a consequence of combined afferent vasodilation (modulation of tubuloglomerular feedback, TGF) and efferent vasoconstriction (activation of renin angiotensin‐aldosterone system, RAAS). AVP positively influences renal sodium absorption at the levels of thick‐ascending limb and distal tubules. It also increases urea cycling and intramedullary urea retention by upregulating urea transporters A1 (UT‐A1) and A3 (UT‐A3) expression. (C) AVP V₂ receptor‐mediated regulation of aquaporin 2 (AQP2) and ENaC. Additionally, hypertonicity of extracellular fluids can efficiently activate tonicity response element binding protein (TonEBP) which upregulates AQP2 expression (independent of AVP). TonEBP also upregulates the expression of osmoprotective genes in the renal epithelial cells, critical in preserving medullary structural integrity.