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Sympathetic Vasoconstriction is Attenuated in Young Women During Hypoxia and Cold Pressor Test
Author(s) -
Ross Amanda J.,
Muller Matthew D.,
Luck J. Carter,
Cui Jian,
Sinoway Lawrence I.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1001.2
Subject(s) - cold pressor test , vasoconstriction , medicine , hypoxia (environmental) , vascular resistance , blood pressure , heart rate , young adult , femoral artery , cardiology , oxygen , chemistry , organic chemistry
Recent studies suggest that muscle sympathetic nerve activity (MSNA) at rest is correlated to vascular resistance in young men but not in young women. We hypothesized that increases in MSNA during acute physiological stressors induce less vasoconstriction in young women compared to young men. Nineteen healthy humans participated in this study (5 young women, 5 young men, 5 older men, 4 older women). Subjects underwent poikilocapnic hypoxia (5 min, 10% O 2 , 90% N 2 ) and the cold pressor test (hand in ice water at 0° C for 2 min). MSNA, femoral blood velocity, heart rate, and blood pressure were acquired continuously. Femoral artery diameter was obtained every minute and used to calculate femoral blood flow (FBF) and vascular resistance (FVR). In response to hypoxia, young women had a similar increase in MSNA compared to young men (Δ 6 ± 1 vs. Δ 7 ± 2, bursts/min, P = 0.632) but an exaggerated increase in FBF (Δ 67 ± 10 vs. Δ 32 ± 14 mL/min, P = 0.031) and a greater reduction in FVR (45 ± 4% vs. 24 ± 9%, P = 0.050). In response to cold pressor test, young women had an attenuated rise in MSNA (Δ 5 ± 1 vs. Δ 26 ± 3, bursts/min, P = 0.008) and a smaller increase in FVR (8 ± 17% vs. 173 ± 48%, P = 0.037) compared to young men. Physiological responses to hypoxia and cold pressor test were comparable between older men and women ( P > 0.1). These data suggest that young women have decreased sympathetic vasoconstrictor drive during physiological stress, which may explain decreased cardiovascular risk. Support or Funding Information UL1 TR000127, KL2 TR000126, P01 HL096570, 15PRE24470033