We have recently shown that estrogen enhances baroreceptor control of refle
x bradycardia in conscious rats. The present study replicated this finding
in pentobarbital sodium-anesthetized rats, and the study was extended to in
vestigate whether this effect of estrogen is centrally or peripherally medi
ated. Hemodynamic responses to electrical stimulation of the central end of
the aortic depressor or the vagal efferent nerve were evaluated in pentoba
rbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OV
X estradiol-treated Sprague-Dawley rats. Phenylephrine (1-16 mu g/kg iv) el
icited dose-dependent presser and bradycardic responses. Regression analysi
s of the baroreflex curves, relating changes in mean arterial pressure and
heart rate, revealed a significantly smaller baroreflex sensitivity in OVX
compared with SO anesthetized rats (-0.54 +/- 0.05 and -0.91 +/- 0.12 beats
.min(-1).mmHg(-1), respectively; P < 0.05). Treatment of OVX rats with 17 b
eta-estradiol (E-2, 50 mu g.kg(-1).day(-1) for 2 days subcutaneously) signi
ficantly enhanced baroreflex sensitivity to a level similar to that of SO r
ats (P < 0.05). The enhancing effect of E-2 on the baroreflex-mediated brad
ycardia, observed in conscious and anesthetized rats, seems to be selective
because the baroreflex-mediated tachycardic responses measured in a separa
te group of conscious rats were not altered by ovariectomy or Ea administra
tion. Electrical stimulation of the aortic nerve elicited frequency-depende
nt depressor and bradycardic responses that were significantly smaller in O
VX compared with SO values (P < 0.05). Treatment of OVX rats with E-2 resto
red the hemodynamic responses to aortic stimulation to near SO levels. On t
he other hand, hemodynamic responses to vagal stimulation were not affected
by OVX or treatment with E-2. These findings suggest that enhancement of r
eflex bradycardia by estrogen is centrally mediated and involves interactio
n with central projections of the aortic nerve.