Desmopressin is a synthetic analogue of vasopressin, which has little effect on the V1 receptors. It is almost a pure antidiuretic. It is also the only drug useful for treatment of platelet dysfunction induced by clopidogrel, aspirin, NSAIDs in general, and uraemia. One can read more about this use of DDAVP in this 1997 article by Pier Manucci. But, you haven't got all day. So, in brief:

• Apparently, the mechanism of action si mainly to do with release of autologous factors. Desmopressin acts on storage sites in vascular endothelium, rapidly releasing stored vWF and Factor VIII. The storage bodies are called Weibel-Palade bodies (Normally, von Willebrand Factor and factor VIII are bound together and circulate around as a soluble complex). As a result, the APPT should decrease.
• Thus, desmopressin has some efficacy for the treatment of "mild" von Willbrand disease, and mild haemophilia.
• The effects of DDAVP in uraemia have been studied (also Manucci et al, 1983) and the improvement in bleeding time seemed to be proportional to the increaded Factor VIII activity. However, subsequent studies (Colucci et al, 2014)have abundantly demonstrated  that it also does a bunch of other useful things to platelet aggregation:
  • Increases the density of platelet surface glycoprotein receptors
  • Enhances the ability to form procoagulant platelets and increases platelet-dependent thrombin generation by enhancing Na⁺/Ca²⁺ mobilization.
  • Thus, increases platelet aggregation
  • Also, increase activity of tissue plasminogen activator antigen.
  • It is not a blood product, and can be used in bleeding Jehovah's witnesses
• The dose required for such effects is actually quite high. The authors gave their patients 0.3 μg/kg body weight over 30 minutes,  in 100 mL 0.9% NaCl