A potential novel strategy, inhibition of vasopressin-induced VEGF secretion by relcovaptan, for decreasing the incidence of ovarian hyperstimulation syndrome in the hyperstimulated rat model

ObjectiveTo investigate the effects of V1A receptor antagonist through inhibition of vasopressin-induced VEGF secretion in an experimental model.Study designThirty rats were randomly divided into five groups. Four groups were given 10 IU pregnant mare serum gonadotropin/day (sc) at 8:00–8:30 am on days 22–25 of life. They were administered 30 IU hCG at 8:00–8:30 am on day 26 of life. On days 26 and 27 of life at 8:00 am and 4:00 pm, (ip) per animal, 50 μg/kg/day GnRH antagonist in the GnRH antagonist group, 0.3 mg relcovaptan in the high dose relcovaptan group, and 0.15 mg relcovaptan in the low dose relcovaptan group were administered. The control group was given the same dosage of 0.9% saline solution (ip) on days 22–26 day of life. The main outcomes were weight gain, ovarian weights, peritoneal fluid VEGF values, corpus luteum count, and atretic follicle count.ResultsWeight gain was highest in the OHSS group; it was almost twice as much in the OHSS group than it was in the control group. Ovarian weights were significantly lower in all treatment groups (p = 0.03). There was no statistically significant difference in ovarian weights between the GnRH antagonist and relcovaptan groups (p = 0.176). The evaluation of peritoneal fluid VEGF-A levels revealed statistically significant differences between levels in the treatment groups and in the OHSS group (p = 0.005). Atretic follicle count in the OHSS group was significantly lower (p = 0.048). In all treatment groups, CL counts were prominently lower than they were in the OHSS group (p = 0.002).ConclusionRelcovaptan may be a novel strategy for decreasing risk of OHSS by inhibition of vasopressin-induced VEGF secretion through V1A receptor antagonist.