V2-receptor blockade enhances pressor response to vasopressin: gender difference

The present study was performed to determine if the attenuated pressor response to vasopressin in conscious non-estrous female rats is due in part to an enhanced V2-like receptor vasodilator action. In male rats, infusion of vasopressin at a rate of 1 ng.min(-1).kg body weight-1 (wt) resulted in an increase in mean arterial blood pressure (MABP) of about 20 mm Hg. Thirty minutes after beginning the infusion of vasopressin, the iv bolus injection of a non-peptide V2-receptor antagonist, OPC-31260 (2 mg.kg body wt-1), resulted in a further gradual increase in MABP of approximately 8 mm Hg in the next 60 min (p < 0.05). Thus, the pressor response to vasopressin was greater in OPC-31260-treated than in vehicle-treated male rats (p < 0.01). The pressor response to vasopressin 30 min after the start of its infusion was lower (about 8 mm Hg) in non-estrous female rats than in males. During the next 60 min of vasopressin infusion, there was a small further increase (p < 0.05) in MABP in the females given either OPC-31260 or its saline vehicle. In contrast to the male rats, however, there was no difference in MABP between the OPC-31260 and vehicle treated females. Thus, the present study has provided additional evidence for a V2-like receptor related vasodilator effect in male rats. However, since female rats do not appear to express a V2-receptor mediated vasodilator response, the sexually dimorphic pressor response to vasopressin cannot be due to a gender difference in V2-receptor vasodilator activity.