Racial differences in resting end-tidal CO2 and circulating sodium pump inhibitor
Previous studies have shown that high end-tidal CO2 (PetCO2) is a marker for sodium sensitivity of blood pressure (BP) in White Americans, and that the BP of African Americans is more sensitive to high sodium intake than that of whites. The present study tested the hypothesis that resting PetCO2 is...
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Veröffentlicht in: | American journal of hypertension 2001-08, Vol.14 (8), p.761-767 |
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Zusammenfassung: | Previous studies have shown that high end-tidal CO2 (PetCO2) is a marker for sodium sensitivity of blood pressure (BP) in White Americans, and that the BP of African Americans is more sensitive to high sodium intake than that of whites. The present study tested the hypothesis that resting PetCO2 is higher in normotensive African Americans than in whites. Resting end-tidal CO2 of 395 white and 125 African American participants in the Baltimore Longitudinal Study on Aging was monitored for 20 min with a respiratory gas monitor, and BP and heart rate were recorded every 5 min by oscillometric methodology. Twenty-four-hour urinary excretion of a circulating sodium pump inhibitor marinobufagenin-like compound (MBG), which increases when plasma volume is expanded, was also analyzed by fluoroimmunoassay in racial groups. Mean resting PetCO2 of African American men was higher than that of white men (38.1 ± 0.5 v 36.4 ± 0.3 mm Hg), and resting PetCO2 of African American women was higher than that of white women (37.7 ± 0.3 v 36.2 ± 0.3 mm Hg). The differences were not significant in either men or women less than 50 years old, but were substantial in both men and women more than 50 years. Twenty-four-hour urinary excretion of MBG was higher in white (2.7 ± 0.2 pmol) than in African American (2.1 ± 0.2 pmol) participants, and high PetCO2 was a significant independent predictor of high MBG excretion in African Americans. These data are consistent with the hypothesis that the higher resting PetCO2 in African Americans plays a role in slower urinary excretion of sodium, greater BP sensitivity to high sodium intake, and increased prevalence of chronic hypertension. Am J Hypertens 2001;14:761–767 © 2001 American Journal of Hypertension, Ltd. |
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ISSN: | 0895-7061 1941-7225 1879-1905 |
DOI: | 10.1016/S0895-7061(01)02163-X |