Estrogen enhancement of baroreflex sensitivity is centrally mediated

Citation
Mk. Mohamed et al., Estrogen enhancement of baroreflex sensitivity is centrally mediated, AM J P-REG, 45(4), 1999, pp. R1030-R1037
Citations number
38
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
45
Issue
4
Year of publication
1999
Pages
R1030 - R1037
Database
ISI
SICI code
0363-6119(199904)45:4<R1030:EEOBSI>2.0.ZU;2-C
Abstract
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.