From:  Physiological basis of arginine vasopressin deficiency (AVP-D, formerly central diabetes insipidus) and AVP-resistance (AVP-R, formerly nephrogenic diabetes insipidus)
 

Molecular and cellular basis of pharmacological interventions of AVP-D and AVP-R

Pharmacological interventionMechanism of actionReference
AVP replacement (desmopressin)Mimics AVP function at V2 receptors, activating the cAMP-PKA pathway, leading to the mobilization of AQP-2 channels, allowing water reabsorption in the kidneys.[61]
Thiazide diureticsIndirectly increase water reabsorption by altering sodium handling in the nephron, which reduces the load on the distal tubules where AVP usually exerts its effects.[63]
AmilorideBlocks ENaC channels, preventing lithium-induced damage to the AVP signaling pathway, thereby preserving AQP-2 channel activity and promoting water reabsorption.[64]
NSAIDsInhibit prostaglandin synthesis, which reduces the antagonistic effect of prostaglandins on AVP, enhancing the hormone’s water-conserving action in the kidneys.[65]
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AQP-2: aquaporin-2; AVP: arginine vasopressin; AVP-D: AVP deficiency; AVP-R: AVP resistance; cAMP-PKA: cyclic adenosine monophosphate-protein kinase A; ENaC: epithelial sodium channels; NSAIDs: non-steroidal anti-inflammatory drugs; V2: vasopressin 2