| Inhibition Signals | Low ‣ → turn on ADH | Urine Osmolarity should be high |
|---|---|---|
| Stimulation Signals | High‣ → turn off ADH | Urine Osmolarity should be low |
<aside>
High Urine Osmolarity means that ADH has been turned ON
</aside>
| Receptor | Type | Location | G-protein pathway | Major function |
|---|---|---|---|---|
| V₁ (V₁a subtype) | GPCR | Vascular smooth muscle, liver, platelets | Gq → IP₃/DAG → ↑ Ca²⁺ | Vasoconstriction, ↑ BP |
| V₂ | GPCR | Principal cells of collecting duct (kidney), vascular endothelium | Gs → ↑ cAMP → PKA | Water reabsorption, ↑ aquaporin-2 insertion; also ↑ vWF & Factor VIII release from endothelium |
| Drug / condition | Mechanism | Predominant receptor |
|---|---|---|
| ‣ | Synthetic ADH analog selective for V₂ | Treats central diabetes insipidus, nocturnal enuresis, vWF disease |
| ‣ | Acts on both V₁ and V₂ | Used in septic shock (V₁) and some bleeding disorders (V₂) |
| ‣ / ‣ | ADH Antagonist | Treat hyponatremia in SIADH |
| ‣ | Excess ADH → V₂ overstimulation | ‣ | Water retention, hyponatremia |
|---|---|---|---|
| ‣ | Absent ADH → V₂ underactivity | ‣ | Water loss, hypernatremia |
| ‣ | V₂ receptor or AQP2 defect | ‣ + normal ‣ | Same labs, but ADH normal/high |