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Baroreflex Function in Young Women with a Family History of Hypertension
Author(s) -
Sebzda Kelly,
Matthews Evan,
Wenner Megan
Publication year - 2015
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.29.1_supplement.648.1
Subject(s) - baroreflex , medicine , blood pressure , cardiology , valsalva maneuver , heart rate , family history
A positive family history of hypertension (+FH) is a risk factor for the future development of hypertension. Reductions in cardiovagal baroreflex sensitivity (BRS) are also associated with hypertension and cardiovascular disease. Therefore, we hypothesized that young women with +FH (n=13, 22±1 yrs, 21±1 kg/m 2 , 84±2 mmHg resting mean blood pressure (BP)) would have lower BRS compared to young women without a family history of hypertension (‐FH; n=11, 21±1 yrs, 22±1 kg/m 2 , 81±3 mmHg resting mean BP, all P >0.05 between groups). We examined BRS as the relationship between systolic BP and R‐R intervals during phases II and IV of the Valsalva maneuver. The slope of the relationship between systolic BP and R‐R interval was determined using linear regression, and used as an index of cardiovagal BRS. We accepted linear regressions with an r > 0.70 for analysis. Cardiovagal BRS was similar during phase II of the Valsalva maneuver (Mean slope: +FH 6.1±0.8 vs. ‐FH 6.4±1.6, P =0.87). However, cardiovagal BRS during phase IV of the Valsalva maneuver tended to be lower in the +FH group (+FH n=10, ‐FH n=8, mean slope: +FH 9.3±2.2 vs. ‐FH 15.3±2.2, P =0.07). Mean BP (+FH 80±1 mmHg, ‐FH 78±2 mmHg) and resting heart rate (+FH 63±3 bpm, ‐FH 66±2 bpm) during the experimental visit were similar between groups. These preliminary data suggest that women with a positive family history of hypertension may have reduced cardiovagal BRS. This may be one mechanism contributing to the development of future hypertension in those with a family history. This work was supported in part by NIH Grant U54‐GM104941 (PI: Binder‐Macleod).