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This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1063    most recent 01163.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Pamidimukkala, J. Articles by Hay, M. Search for Related Content PubMed PubMed Citation Articles by Pamidimukkala, J. Articles by Hay, M.

Estrogen receptor- mediates estrogen facilitation of baroreflex heart rate responses in conscious mice

¹Dalton Cardiovascular Research Center, ²Department of Veterinary Biomedical Sciences, ³Center for Gender Physiology, ⁴Department of Biochemistry and Child Health, ⁵University of Missouri Center for Phytonutrient and Phytochemical Studies, University of Missouri, Columbia, Missouri

Submitted 9 December 2003 ; accepted in final form 6 November 2004

Estrogen facilitates baroreflex heart rate responses evoked by intravenous infusion of ANG II and phenylephrine (PE) in ovariectomized female mice. The present study aims to identify the estrogen receptor subtype involved in mediating these effects of estrogen. Baroreflex responses to PE, ANG II, and sodium nitroprusside (SNP) were tested in intact and ovariectomized estrogen receptor- knockout (ERKO) with (OvxE+) or without (OvxE–) estrogen replacement. Wild-type (WT) females homozygous for the ER^+/+ were used as controls. Basal mean arterial pressures (MAP) and heart rates were comparable in all the groups except the ERKO-OvxE+ mice. This group had significantly smaller resting MAP, suggesting an effect of estrogen on resting vascular tone possibly mediated by the ER subtype. Unlike the WT females, estrogen did not facilitate baroreflex heart rate responses to either PE or ANG II in the ERKO-OvxE+ mice. The slope of the line relating baroreflex heart rate decreases with increases in MAP evoked by PE was comparable in ERKO-OvxE– (–6.97 ± 1.4 beats·min^–1·mmHg^–1) and ERKO-OvxE+ (–6.18 ± 1.3) mice. Likewise, the slope of the baroreflex bradycardic responses to ANG II was similar in ERKO-OvxE– (–3.87 ± 0.5) and ERKO-OvxE+(–2.60 ± 0.5) females. Data suggest that estrogen facilitation of baroreflex responses to PE and ANG II is predominantly mediated by ER subtype. A second important observation in the present study is that the slope of ANG II-induced baroreflex bradycardia is significantly blunted compared with PE in the intact as well as the ERKO-OvxE+ females. We have previously reported that this ANG II-mediated blunting of cardiac baroreflexes is observed only in WT males and not in ovariectomized WT females independent of their estrogen replacement status. The present data suggest that in females lacking ER, ANG II causes blunting of cardiac baroreflexes similar to males and may be indicative of a direct modulatory effect of the ER on those central mechanisms involved in ANG II-induced resetting of cardiac baroreflexes. These observations suggest an important role for ER subtype in the central modulation of baroreflex responses. Lastly, estrogen did not significantly affect reflex tachycardic responses to SNP in both WT and ERKO mice.

autonomic regulation; cardiac baroreflexes; hormone replacement; angiotensin II

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