Estrogen enhancement of baroreflex sensitivity is centrally mediated.
We have recently shown that estrogen enhances baroreceptor control of reflex bradycardia in conscious rats. The present study replicated this finding in pentobarbital sodium-anesthetized rats, and the study was extended to investigate whether this effect of estrogen is centrally or peripherally mediated. Hemodynamic responses to electrical stimulation of the central end of the aortic depressor or the vagal efferent nerve were evaluated in pentobarbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OVX estradiol-treated Sprague-Dawley rats. Phenylephrine (1-16 microgram/kg iv) elicited dose-dependent pressor and bradycardic responses. Regression analysis 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 17beta-estradiol (E2, 50 microgram. kg-1. day-1 for 2 days subcutaneously) significantly enhanced baroreflex sensitivity to a level similar to that of SO rats (P < 0.05). The enhancing effect of E2 on the baroreflex-mediated bradycardia, observed in conscious and anesthetized rats, seems to be selective because the baroreflex-mediated tachycardic responses measured in a separate group of conscious rats were not altered by ovariectomy or E2 administration. Electrical stimulation of the aortic nerve elicited frequency-dependent depressor and bradycardic responses that were significantly smaller in OVX compared with SO values (P < 0.05). Treatment of OVX rats with E2 restored the hemodynamic responses to aortic stimulation to near SO levels. On the other hand, hemodynamic responses to vagal stimulation were not affected by OVX or treatment with E2. These findings suggest that enhancement of reflex bradycardia by estrogen is centrally mediated and involves interaction with central projections of the aortic nerve.
Mohamed
M K
MK
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.
El-Mas
M M
MM
Abdel-Rahman
A A
AA
D000818:Animals; D001011:Aorta / Q000294:innervation; D017704:Baroreflex / Q000187:drug effects* / Q000502:physiology*; D001919:Bradycardia / Q000139:chemically induced / Q000503:physiopathology; D001921:Brain / Q000502:physiology*; D004558:Electric Stimulation; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D009424:Nervous System Physiological Phenomena; D009599:Nitroprusside; D010052:Ovariectomy; D010656:Phenylephrine; D051381:Rats; D017207:Rats, Sprague-Dawley; D013610:Tachycardia / Q000139:chemically induced / Q000503:physiopathology; D014630:Vagus Nerve / Q000502:physiology
D009599:Nitroprusside; D010656:Phenylephrine; D004958:Estradiol