i don't think its talking about ADH release, i think they are talking about potentiating the effect of ADH so like helping it to bind to the receptor. It wouldn't really make sense to say that indomethacin helps with ADH release since indomethacin is used for nephrogenic DI which is a problem with the ADH receptor not the release of ADH (that would be central DI).
From Uptodate: Nonsteroidal anti-inflammatory drugs — The efficacy of NSAIDs in this setting is dependent upon inhibition of renal prostaglandin synthesis. In normal subjects, prostaglandins antagonize the action of ADH and NSAIDs increase concentrating ability [
26,27]. If, for example, normal subjects are given a submaximal dose of ADH, the ensuing rise in urine osmolality can be increased by more than 200 mosmol/kg if the patient has been pretreated with a NSAID [
26]. The net effect in patients with DI may be a 25 to 50 percent reduction in urine output [
16,17,28], a response that is partially additive to that of a thiazide diuretic [
17,19].
This approach is particularly beneficial in patients with polyuria due to complex congenital polyuric-polydipsic Bartter-like syndromes, in whom prostaglandins appear to be pathogenetically important. (See
"Bartter and Gitelman syndromes", section on 'Role of prostaglandins'.)
Not all NSAIDs are equally effective in a given patient; as an example,
indomethacin appears to have a greater effect than
ibuprofen [
16]. A variety of complications may ensue with long-term use of NSAIDs. (See
"Nonselective NSAIDs: Overview of adverse effects".)
Exogenous ADH — Most patients with
non-hereditary nephrogenic DI have partial rather than complete resistance to ADH. It is therefore possible that attaining supraphysiologic hormone levels will increase the renal effect of ADH to a clinically important degree. In some patients with nephrogenic DI, exogenous ADH has been found to increase the urine osmolality by 40 to 45 percent, an effect that would be expected to produce a similar decline in urine volume [
20,29,30].
Thus,
desmopressin (dDAVP) may be tried in patients who have persistent symptomatic polyuria after implementation of the above regimen. One case report of a patient with
lithium-induced nephrogenic DI suggested that benefit may be more likely if desmopressin is combined with a NSAID [
31].
