End tidal CO2 is an independent determinant of systolic blood pressure in women

Citation
De. Anderson et al., End tidal CO2 is an independent determinant of systolic blood pressure in women, J HYPERTENS, 17(8), 1999, pp. 1073-1080
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
02636352 → ACNP
Volume
17
Issue
8
Year of publication
1999
Pages
1073 - 1080
Database
ISI
SICI code
0263-6352(199908)17:8<1073:ETCIAI>2.0.ZU;2-O
Abstract
Objective Recent studies have shown that high resting end tidal CO2 (PECO2) is a marker for blood pressure sensitivity to high sodium intake by normot ensive humans. The present study investigated the association of resting PE CO2 with resting blood pressure in participants in the Baltimore Longitudin al Study on Aging (BLSA). Design PECO2 of 314 healthy participants (153 men and 161 women, aged 21 -7 9 years) was measured by a respiratory gas monitor during 25 min of seated rest, and blood pressure every 5 min by an automated oscillometric system. The independent associations of PECO2 and other variables with systolic (SB P) and diastolic (DBP) blood pressure were analysed via multiple regression . Sex differences in age-associated changes in PECO2 and in the role of pul monary capacity in the PECO2 - blood pressure relationships were also studi ed. Results Resting PECO2 was an independent predictor of SEP in women (beta = 0.215; P < 0.0015; overall r(2) = 0.27; P < 0.0001), and accounted for more than 10% of the variance in SEP in women over age 50 years. No such associ ations of PECO2 with SEP of men, or with DBP of men or women, were observed , PECO2 was lower in younger women (36.0 +/- 0.9 mmHg) than in younger men (40.4 +/- 2.0), but higher in older women (37.1 +/- 0.5) than in older men (35.5 +/- 0.4). Conclusions PECO2 is an independent determinant of resting SEP in women, es pecially those aged 50 years or more. The origin of individual differences in resting PECO2 and its possible role in the development of chronic hypert ension remain to be clarified. J Hypertens 1999, 17:1073-1080 (C) Lippincot t Williams & Wilkins.