Blood pressure responses to handgrip exercise but not apnea or mental stress are enhanced in women with a recent history of preeclampsia
- PMID: 38700469
- PMCID: PMC11932533
- DOI: 10.1152/ajpheart.00020.2024
Blood pressure responses to handgrip exercise but not apnea or mental stress are enhanced in women with a recent history of preeclampsia
Abstract
Preeclampsia is a risk factor for future cardiovascular diseases. However, the mechanisms underlying this association remain unclear, limiting effective prevention strategies. Blood pressure responses to acute stimuli may reveal cardiovascular dysfunction not apparent at rest, identifying individuals at elevated cardiovascular risk. Therefore, we compared blood pressure responsiveness with acute stimuli between previously preeclamptic (PPE) women (34 ± 5 yr old, 13 ± 6 mo postpartum) and women following healthy pregnancies (Ctrl; 29 ± 3 yr old, 15 ± 4 mo postpartum). Blood pressure (finger photoplethysmography calibrated to manual sphygmomanometry-derived values; PPE: n = 12, Ctrl: n = 12) was assessed during end-expiratory apnea, mental stress, and isometric handgrip exercise protocols. Integrated muscle sympathetic nerve activity (MSNA) was assessed in a subset of participants (peroneal nerve microneurography; PPE: n = 6, Ctrl: n = 8). Across all protocols, systolic blood pressure (SBP) was higher in PPE than Ctrl (main effects of group all P < 0.05). Peak changes in SBP were stressor specific: peak increases in SBP were not different between PPE and Ctrl during apnea (8 ± 6 vs. 6 ± 5 mmHg, P = 0.32) or mental stress (9 ± 5 vs. 4 ± 7 mmHg, P = 0.06). However, peak exercise-induced increases in SBP were greater in PPE than Ctrl (11 ± 5 vs. 7 ± 7 mmHg, P = 0.04). MSNA was higher in PPE than Ctrl across all protocols (main effects of group all P < 0.05), and increases in peak MSNA were greater in PPE than Ctrl during apnea (44 ± 6 vs. 27 ± 14 burst/100 hb, P = 0.04) and exercise (25 ± 8 vs. 13 ± 11 burst/100 hb, P = 0.01) but not different between groups during mental stress (2 ± 3 vs. 0 ± 5 burst/100 hb, P = 0.41). Exaggerated pressor and sympathetic responses to certain stimuli may contribute to the elevated long-term risk for cardiovascular disease in PPE.NEW & NOTEWORTHY Women with recent histories of preeclampsia demonstrated higher systolic blood pressures across sympathoexcitatory stressors relative to controls. Peak systolic blood pressure reactivity was exacerbated in previously preeclamptic women during small muscle-mass exercises, although not during apneic or mental stress stimuli. These findings underscore the importance of assessing blood pressure control during a variety of experimental conditions in previously preeclamptic women to elucidate mechanisms that may contribute to their elevated cardiovascular disease risk.
Keywords: blood pressure; muscle sympathetic nerve activity; postpartum; preeclampsia; pressor responses.
Conflict of interest statement
N. S. Stachenfeld serves as principal investigator on National Institutes of Health (NIH) Grant R01HL135089 and coprincipal investigator on NIH Grants R01HL161000 and R21HD107609.
M. J. Paidas discloses the following: received grant funding as principal investigator from GestVision, Inc., for a study evaluating a novel diagnostic urine test for preeclampsia until departing from Yale University in October 2018 but no longer receives this funding; received grant funding from rEVO Biologics, LLC, to conduct a preeclampsia interventional clinical trial but no longer receives this funding; received research funding, while at Yale University, from rEVO Biologics, LLC, to support preeclampsia research via the Yale Women and Children’s Center for Blood Disorders and Preeclampsia Advancement but no longer receives this funding; receives grant funding as principal investigator at University of Miami for an antithrombin replacement clinical trial sponsored by OctaPharma and has received funding for participation in an Advisory Board, sponsored by OctaPharma; receives grant funding as principal investigator at University of Miami for a prospective cohort study regarding fetal neonatal alloimmune thrombocytopenia sponsored by Rallybio; receives research funding and is principal investigator for COVID research sponsored by Muriel, Murray, and Robert Smith Foundation; receives grant funding and is principal investigator for Long COVID research sponsored by Charles M Vallee Foundation; receives funding from the Scaife Family Foundation, as principal investigator a maternal mental health program; team received a grant related to COVID research from the University of Miami as principal investigator for a Neuroscience Team Science Funding Program Award; receives grant funding from BioIncept, LLC, as principal investigator at the University of Miami of an NICHD sponsored preclinical study to evaluate synthetic PreImplantation Factor to treat hypoxic ischemic encephalopathy and serves as a Scientific Advisory Board member with stock options for this role; is a multiple principal investigator of an NIH funded multicenter study (G3 OD035542-01-NIH), entitled Miami ECHO: A diverse Cohort of Mothers, Children, and Fathers in Miami-Dade County; receives royalties as a contributing author from UpToDate; is a Member of the Protocol Expert Panel (Clinical, laboratory, Immunology, -omics), Maternal Fetal Medicine, of an NIH/NHLBI Grant, UG3HL165064, “The Hemophilia An Analytical Cohort Research Program (HARP); An Intergenerational Precision Medicine Research Program for the Study of Factor VIII Immunogenicity in Severe Hemophilia A”; and is a coinvestigator and mentor for an NIH/NHLBI F31 grant (1F1HL 165894-01A1) entitled Hypertensive Disorders of Pregnancy: The Black White Disparity.
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Comment in
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Cardiovascular consequences of preeclampsia: Is the reactivity to stress the missing piece of the puzzle?Am J Physiol Heart Circ Physiol. 2024 Jul 1;327(1):H138-H139. doi: 10.1152/ajpheart.00312.2024. Epub 2024 May 24. Am J Physiol Heart Circ Physiol. 2024. PMID: 38787384 No abstract available.
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