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1 Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
2 Department of Biochemistry and Child Health, University of Missouri, Columbia, MO, USA
3 Center for Gender Physiology, University of Missouri, Columbia, MO, USA; Department of Biochemistry and Child Health, University of Missouri, Columbia, MO, USA; MU center for Phytonutrient and Phytochemical Studies, University of Missouri, Columbia, MO, USA
4 Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, MO, USA; Center for Gender Physiology, University of Missouri, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: PamidimukkalaJ{at}missouri.edu.
Estrogen facilitates baroreflex heart rate responses evoked by intravenous infusion of angiotensin II (ANGII) 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 phenylephrine (PE), angiotensin II (AngII and sodium nitroprusside (SNP) were tested in intact and ovariectomized estrogen receptor alpha knockout (ER
KO) with (OvxE+) or without (OvxE-) estrogen
replacement. 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 HR responses to either PE or ANGII in the ovariectomized ERKO mice. The slope of the line relating baroreflex HR decreases to increases in MAP evoked by PE were comparable in ERKO-OvxE- (-6.97±1.4 bpm/mmHg) and ERKO-OvxE+ (-6.18±1.3) mice. Likewise, the slope of the baroreflex bradycardic responses to ANGII was similar in ERKO-OvxE- (-3.87±0.5) and ERKO-OvxE+(-2.60±0.5) females. The data suggest that estrogen facilitation of baroreflex responses to PE and ANGII are predominantly mediated by ER subtype. A second important observation in the present study is the slope of ANGII induced baroreflex bradycardia is significantly blunted compared to PE in the intact as well as the ovariectomized ERKO. We have previously reported that this ANGII 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, ANGII 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 ANGII 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.
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