issue of Hypertension, Bankir et al 1 analyzed the data of 325 subjects divided into tertiles of the day:night ratio of urinary sodium excretion. Subjects in tertile 3 were qualified as "high daytime sodium excretors" because they excreted sodium at a rate that was 46% higher during daytime than during nighttime, whereas subjects in tertile 1 were "low daytime sodium excretors" and excreted 3 times less sodium during daytime than during nighttime. The nocturnal blood pressure (BP) dipping was

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... gnificantly lower in tertile 1 than in other tertiles, especially for systolic BP. Thus, the authors suggested that the capacity to excrete sodium during daytime is the main determinant of nocturnal BP and dipping. However, the mechanisms associated with the reproducibility of the circadian BP pattern remain to be elucidated. It is well known that when ambulatory BP monitoring (ABPM) is repeated without interventions in the short 2 or long term, 3 a spontaneous change may occur in the nocturnal BP. Thus, we 4 investigated whether individuals with a spontaneous change in the nocturnal BP fall have any differences in physiological mechanisms of BP control. Normotensive and hypertensive subjects underwent two 24-hour ABPM recordings separated by 30 days and also measurements in the same period of plasma renin activity, aldosterone, catecholamines, and 24-hour urinary sodium/potassium excretion. Twenty-three individuals (50%) maintained the same nocturnal systolic and diastolic BP fall profile, "dipper" (nϭ14) or "nondipper" (nϭ9), designated as the "maintained" group. In 23 individuals (50%), the nocturnal BP fall profile changed, from dipper to nondipper (nϭ16) or from nondipper to dipper (nϭ7), called the "changed group." The maintained and changed groups were not different in relation to age, body mass index, gender, plasma renin activity, aldosterone, catecholamines, and 24-hour urinary potassium excretion. However, it was observed that, in the changed group, the subgroup that changed from dipper (ABPM 1) to nondipper (ABPM 2) had a significant increase in nocturnal BP on ABPM 2 (123Ϯ16 to 131Ϯ19 mm Hg; PϽ0.05) and lower urinary sodium excretion (151Ϯ65 versus 112Ϯ48 mEq/24 hours; PϽ0.05) and a negative correlation between the difference in nighttime ambulatory systolic BP (ABPM 1 Ϫ ABPM 2) and in 24-hour urinary sodium excretion (rϭϪ0.63; Pϭ0.01). A explanation for this finding could be that the subjects in this subgroup probably had an elevation in nocturnal systolic BP during the second 24-hour recording because of lower sodium excretion in the daytime, as showed by Bankir et al. 1 For a better understanding of this subject, further studies should be done to investigate the sodium excretion during daytime and nighttime in two 24-hour ABPM recordings.