An in vitro animal model which examines the effects of sex hormone variations during the menstrual cycle on basilar artery reactivity is presented. Three groups of rabbits were utilized: a chronically depleted control group which received no further hormonal treatment after bilateral surgical oophorectomy (O), simulating menopause, and two groups of intact females, one of which was treated to mimic the estrogen and progesterone surge during the luteal phase (H) and the third group which was acutely estrogen and progesterone depleted after the luteal surges to simulate the immediate premenstrual state (W). We show that both acute and chronic estrogen and progesterone withdrawal significantly increase serotonin sensitivity (ED50) in basilar artery rings. There was no difference between groups for maximum contraction (Tmax) to serotonin, nor optimal resting tension. Furthermore, there was no difference in vasoreactivity and contractility to norepinephrine between groups. In order to distinguish between the effects of chronic and acute treatment we examined acute estrogen and progesterone superfusion in basilar artery rings from intact non-treated female rabbits. Acute superfusion of pre-contracted and non-pre-contracted artery segments resulted in significant dilatation only when supraphysiologic concentrations of estrogen and progesterone were used. We conclude that both acute and chronic female sex hormone withdrawal selectively increases cerebral vasoreactivity to serotonin.
