Figure 218

Principal cortical collecting tubule (CCT) cells. In these cells, sodium (Na) enters across the luminal membrane through Na channels (ENaC). The movement of cationic Na from lumen to cell depolarizes the luminal membrane, generating a transepithelial electrical gradient oriented with the lumen negative with respect to intersti-tium. This electrical gradient permits cationic potassium (K) to diffuse preferentially from cell to lumen through K channels (ROMK). Na transport is stimulated when aldosterone interacts with its intracellular receptor [43]. This effect involves both increases in the number of Na channels at the luminal membrane and increases in the number of Na-K ATPase (Sodium-potassium adenosine triphosphatase) pumps at the basolateral cell membrane. Arginine vasopressin (AVP) stimulates both Na absorption (by interacting with V2 receptors and, perhaps, Vj receptors) and water transport (by interacting with V2 receptors) [44-46]. V2 receptor stimulation leads to insertion of water channels (aquapor-in 2) into the luminal membrane [47]. V2 receptor stimulation is modified by PGE2 and <X2 agonists that interact with a receptor that stimulates G( [48]. AC—adenylyl cyclase; ATP—adenosine triphosphate; cAMP—cyclic adenosine monophosphate; CCT—cor-tical collecting tubule; Gi—inhibitory G protein; Gs—stimulatory G protein; R—Ri receptor.

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