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Baroreflex sensitivity correlates with ambulatory average blood pressure and daytime heart rate variability in healthy normotensives
Author(s) -
Hesse Christiane,
Liu Zhong,
Pike Tasha L.,
Charkoudian Nisha,
Joyner Michael J.,
Eisenach John H.
Publication year - 2007
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.21.5.a564-b
Subject(s) - baroreflex , heart rate , blood pressure , medicine , ambulatory , heart rate variability , ambulatory blood pressure , cardiology , mean arterial pressure , anesthesia , sodium nitroprusside , phenylephrine , nitric oxide
Background: Hypertensive patients have blunted arterial baroreflex sensitivity (BRS). In these patients, BRS is positively related to heart rate variability and inversely related to blood pressure (BP) variability. We hypothesized that this relationship would also be evident in healthy normotensives, and that individuals with higher BRS would have lower ambulatory 24‐hour BP. Methods: 24‐hour ambulatory BP and heart rate was recorded using Spacelabs recorders in 53 healthy, normotensive, non‐obese individuals (32 women, 21 men). Furthermore, BRS (baroreflex control of RR‐interval) was assessed with the modified Oxford technique (sequential bolus administration of sodium nitroprusside and phenylephrine). Results: BRS as well as heart rate and BP variabilities varied greatly among participants. Whereas no relation was observed between BRS and 24‐hour heart rate and BP variabilities, BRS was positively correlated to daytime heart rate variability (R=0.324, p=0.018) and inversely to 24‐hour average mean arterial pressure (R=0.400, p=0.003). Conclusion: In normotensive individuals, higher BRS is related to higher heart rate variability during daytime. Furthermore, BRS was inversely related to 24‐hour mean arterial pressure, consistent with the idea that the baroreflex may have more long‐term influences than previously thought. Supported by NIH grants K23 RR17520, HL 46493, DFG grant He 4605/1‐1.