Previous studies have demonstrated augmentation of baroreflex-mediated
bradycardia by arginine vasopressin (AVP). However, the specific rece
ptor subtype responsible for mediating this augmentation has not been
determined. In the present study, experiments were performed in consci
ous rats to determine the possible involvement of oxytocin receptors i
n this response. Infusion of oxytocin at a dose that had no effect on
baseline hemodynamic values significantly augmented the bradycardic re
sponse to IV bolus doses of methoxamine. Prior treatment with selectiv
e antagonists to either oxytocin, V-1 vasopressinergic or V-2 vasopres
sinergic receptors reversed this enhancement. In a separate set of exp
eriments, baroreflex-mediated bradycardic responses to IV bolus doses
of AVP were assessed. Pretreatment with the selective oxytocin recepto
r antagonist reversed vasopressinergic augmentation of baroreflex sens
itivity. Finally, combined vasopressinergic and oxytocinergic stimulat
ion of the baroreflex was assessed. Treatment with both AVP and oxytoc
in did not augment baroreflex-mediated bradycardia greater than AVP al
one. We conclude from these experiments that AVP and oxytocin both aug
ment baroreflex sensitivity, although the receptor type(s) responsible
are not clear.