Table Info

Table 3.

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

Pharmacological intervention	Mechanism of action	Reference
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 diuretics	Indirectly 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]
Amiloride	Blocks ENaC channels, preventing lithium-induced damage to the AVP signaling pathway, thereby preserving AQP-2 channel activity and promoting water reabsorption.	[64]
NSAIDs	Inhibit prostaglandin synthesis, which reduces the antagonistic effect of prostaglandins on AVP, enhancing the hormone’s water-conserving action in the kidneys.	[65]

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

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