The present study was performed to determine if the attenuated presser
response to vasopressin in conscious non-estrous female rats is due i
n part to an enhanced V-2-like receptor vasodilator action. In male ra
ts, infusion of vasopressin at a rate of 1 ng . min(-1). kg body weigh
t(-1) (wt) resulted in an increase in mean arterial blood pressure (MA
BP) of about 20 mm Hg. Thirty minutes after beginning the infusion of
vasopressin, the iv bolus injection of a non-peptide V-2-receptor anta
gonist, OPC-31260 (2 mg . kg body wt(-1)), resulted in a further gradu
al increase in MABP of approximately 8 mm Hg in the next 60 min (p < 0
.05). Thus, the presser response to vasopressin was greater in OPC-312
60-treated than in vehicle-treated male rats (p < 0.01). The presser r
esponse to vasopressin 30 min after the start of its infusion was lowe
r (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 increa
se (p < 0.05) in MABP in the females given either OPC-31260 or its sal
ine vehicle. In contrast to the male rats, however, there was no diffe
rence in MABP between the OPC-31260 and vehicle treated females. Thus,
the present study has provided additional evidence for a V-2-like rec
eptor related vasodilator effect in male rats. However, since female r
ats do not appear to express a V-2-receptor mediated vasodilator respo
nse, the sexually dimorphic presser response to vasopressin cannot be
due to a gender difference in V-2-receptor vasodilator activity.