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1 Dalton Cardiovascular Research Center, University Of Missouri, Columbia, MO, USA
2 Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, MO, USA
3 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
* To whom correspondence should be addressed. E-mail: PamidimukkalaJ{at}missouri.edu.
It has been suggested that estrogen modulates baroreflex regulation of autonomic function. The present study evaluated the effects of estrogen on baroreflex regulation of heart rate in response to changes in blood pressure with phenylephrine (PE), angiotensin II (AngII) and sodium nitroprusside (SNP) in a conscious mouse model. Males and ovariectomized females with (OvxE+) and without (OvxE-) estradiol replacement, chronically implanted with arterial and venous catheters were used in these studies. The slope of the baroreflex bradycardic responses to PE was significantly facilitated in OvxE+ females (-7.65±1.37) compared to OvxE- females (-4.5±0.4). Likewise, the slope of the baroreflex bradycardic responses to AngII was significantly facilitated in OvxE+ females (-7.97±1.06) compared to OvxE- females (-4.8±1.6). Reflex tachycardic responses to SNP were comparable in all the groups. Lastly, in male mice, the slope of AngII induced baroreflex bradycardia (-5.17±0.95) was significantly less than that induced by PE (-8.50±0.92), but this AngII mediated attenuation of reflex bradycardia was not observed in the female mice. These data support the hypothesis that estrogen facilitates baroreflex function in female mice and suggest that AngII mediated acute blunting of baroreflex regulation of heart rate may be sex dependent.
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