title: Short-term administration of progesterone and estradiol independently alter carotid-vasomotor, but not carotid-cardiac, baroreflex function in young women.
abstract: The individual effects of estrogen and progesterone on baroreflex function remain poorly understood. We sought to determine how estradiol (E2) and progesterone (P4) independently alter the carotid-cardiac and carotid-vasomotor baroreflexes in young women by using a hormone suppression and exogenous add-back design. Thirty-two young women were divided into two groups and studied under three conditions: 1) after 4 days of endogenous hormone suppression with a gonadotropin releasing hormone antagonist (control condition), 2) after continued suppression and 3 to 4 days of supplementation with either 200 mg/day oral progesterone (N = 16) or 0.1 to 0.2 mg/day transdermal 17β-estradiol (N = 16), and 3) after continued suppression and 3 to 4 days of supplementation with both hormones. Changes in heart rate (HR), mean arterial pressure (MAP), and femoral vascular conductance (FVC) were measured in response to 5 s of +50 mmHg external neck pressure to unload the carotid baroreceptors. Significant hormone effects on the change in HR, MAP, and FVC from baseline at the onset of neck pressure were determined using mixed model covariate analyses accounting for P4 and E2 plasma concentrations. Neither P4 (P = 0.95) nor E2 (P = 0.95) affected the HR response to neck pressure. Higher P4 concentrations were associated with an attenuated fall in FVC (P = 0.01), whereas higher E2 concentrations were associated with an augmented fall in FVC (P = 0.02). Higher E2 was also associated with an augmented rise in MAP (P = 0.01). We conclude that progesterone blunts whereas estradiol enhances carotid-vasomotor baroreflex sensitivity, perhaps explaining why no differences in sympathetic baroreflex sensitivity are commonly reported between low and high combined hormone phases of the menstrual cycle.
authors.affiliation: Department of Human Physiology, University of Oregon, Eugene, Oregon;
authors.forename: Vienna E
authors.initials: VE
authors.lastname: Brunt
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Miner
authors.forename: Paul F
authors.initials: PF
authors.lastname: Kaplan
authors.forename: John R
authors.initials: JR
authors.lastname: Halliwill
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Strycker
authors.forename: Christopher T
authors.initials: CT
authors.lastname: Minson
mesh_terms: D000279:Administration, Cutaneous; D000284:Administration, Oral; D000367:Age Factors; D000704:Analysis of Variance; D062186:Arterial Pressure / Q000187:drug effects; D017704:Baroreflex / Q000187:drug effects*; D002339:Carotid Arteries / Q000294:innervation*; D004334:Drug Administration Schedule; D004958:Estradiol / Q000008:administration & dosage* / Q000097:blood; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000008:administration & dosage / Q000031:analogs & derivatives; D006321:Heart / Q000294:innervation*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006727:Hormone Antagonists / Q000008:administration & dosage; D006801:Humans; D016014:Linear Models; D011311:Pressoreceptors / Q000187:drug effects* / Q000378:metabolism; D011374:Progesterone / Q000008:administration & dosage* / Q000097:blood; D012737:Sex Factors; D013997:Time Factors; D057968:Transdermal Patch; D014666:Vasomotor System / Q000187:drug effects*; D055815:Young Adult
chemical_list: D006727:Hormone Antagonists; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; C061018:ganirelix
keywords: arterial baroreceptors; blood pressure; estrogen; hormones; menstrual cycle