Table 2: Summary of investigations supporting a role for EC33 and PC18 (EC27) in blocking the release of vasopressin and controlling hypertension in animal models.

PreparationFindingReference

Synthesis of EC33Designed by Chauvel as a specific inhibitor of APA [111]
Synthesized by Reaux and colleagues
i.c.v. infusion-miceEC33 increased the half-life of [3H]AngII by 2.6 fold and blocked the formation of [3H]AngIII[108]
PC18 and EC27 increased the half-life of [3H]AngIII by 3.9 and 2.3 fold, respectively[108, 111]
EC33 reduced AngII-induced vasopressin release in a dose-response-dependent fashion[111]
Injection of PC18 and EC27 increased vasopressin release[111]
Normotensive ratsRecorded from vasopressinergic neurons in the SON
(urethane-anesth.)i.c.v. infusion of AngII and AngIII significantly increased firing rate. i.c.v. infusion of EC33 abruptly stopped firing rate for 4–6 min. i.c.v. infusion of AngII followed by EC33 prevented the increase in firing rate to AngII[112]
i.c.v. infusion-SHRsEC33 blocked AngII-induced pressor responses[105, 113]
i.c.v. infusion-normotensive ratsEC33 blocked the pressor response induced by AngII and D-Asp1AngII but had no effect on the pressor responses induced by AngIII or D-Arg1AngIII. PC18 extended the duration of the D-Asp1AngII-induced pressor response 2.5 fold, and the duration of the D-Arg1 AngIII-induced pressor response by 10 to 15 fold. Pretreatment with Losartan blocked these pressor responses, indicating AT1 receptor involvement[91]
Synthesis of RB150Designed by Fournie-Zaluski[107]
DOCA-salt ratsIntravenous administration of RB150 significantly reduced BP for 24 hours[107]
Oral administration of RB150 significantly reduced BP for 7 hours[114, 115]