Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 302, Issue 12, Pages H2560-H2566Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00579.2011
Keywords
baroreflex control; estrogen; progesterone; ambulatory blood pressure; autonomic nervous system; cold pressor test
Funding
- Tobacco-Related Disease Research Program Exploratory/Developmental Research Award [18XT-00115]
- National Institutes of Health (NIH) (University of California, Los Angeles General Clinical Research Center) [MO1-RR-00865]
- NIH [K23-HL-098744]
- Atlanta Research and Education Foundation
- Amgen Junior Faculty
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Middlekauff HR, Park J, Gornbein JA. Lack of effect of ovarian cycle and oral contraceptives on baroreceptor and nonbaroreceptor control of sympathetic nerve activity in healthy women. Am J Physiol Heart Circ Physiol 302: H2560-H2566, 2012. First published April 27, 2012; doi:10.1152/ajpheart.00579.2011.-Endogenous and exogenous female hormones regulate sympathetic nerve activity (SNA) in animal models, but their impact in humans is controversial. The purpose of this study is to investigate the effects of the ovarian cycle and oral contraceptive pills (OCPs) on SNA. We hypothesized that the effects of endogenous hormones were baroreflex (BR)-mediated and that these cyclical changes in BR control were blunted by OCPs. Furthermore, we hypothesized that the nocturnal fall in blood pressure (BP) (dipping), which is sympathetically mediated, also varied with the ovarian cycle. In 23 healthy females (13 OCP users, 10 age-matched, no OCPs), SNA was recorded (microneurography) at rest, during BR activation/deactivation, and cold pressor test (CPT) during low and high hormonal phases. Furthermore, 24-h BP monitoring was performed during low and high hormonal phases. SNA was lower during the low vs. high hormone phase in non-OCP users (17.3 +/- 2.4 vs. 25.4 +/- 3.2 bursts/min, P < 0.001) but was not different between phases in OCP users [15.5 +/- 1.7 vs. 16.6 +/- 2.0 bursts/min, P = not significant (NS)]. BR control of SNA was not different during the hormone phases in either group [SNA (total activity/min) mean slope % change from baseline, no OCP users, low vs. high hormone phase 35.4 +/- 6.2 vs. 29.6 +/- 3.4%, P = NS and OCP users, low vs. high hormone phase 35.7 +/- 3.9 vs. 33.5 +/- 3.5%, P = NS]. SNA activation during CPT was not impacted by hormonal phase or OCP use. Finally, nondipping was not different between OCP users and nonusers, although there was a trend for nondipping to occur more frequently in the OCP users. SNA varies during the ovarian cycle in women in the absence of OCPs. This modulation cannot be attributed to cyclical changes in the BR sensitivity.
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