Short-term low salt intake significantly reduced arterial pressure (P<0.01), but individual responses were variable and the reproducibility of classifying patients as salt-sensitive or -resistant was low.
RCT (n=14)
random order
Does 1 week of low salt intake (40 mmol/day) reproducibly reduce arterial pressure compared to high salt intake (170 mmol/day) in untreated patients with mild essential hypertension?
While short-term low salt intake reduces blood pressure in mild essential hypertension, individual responses are highly variable and classifying patients as salt-sensitive or resistant is poorly reproducible.
BACKGROUND: The reproducibility of the arterial pressure response to change in salt intake in essential hypertensives has been little investigated. OBJECTIVE: To study the reproducibility of the response to salt in 14 untreated patients with mild essential hypertension. METHODS: After a run-in phase (1 month), each patient ingested, in random order and with cross-over, 1 week of high salt intake (170 mmol/day) and 1 week of low salt intake (40 mmol/day). The identical experimental protocol was then repeated after an average interval of 3.4 months. Arterial pressure was measured (clinic arterial pressure and 24 h ambulatory monitoring) on the seventh day of each diet period. The reproducibility of the arterial pressure response was assessed in terms the intraclass correlation coefficient and the K statistics. RESULTS: There was a good compliance with the dietary prescription because the urinary Na excretion was on average very close to the prescribed intake both during the first and during the second salt intake period. Both clinic and 24 h arterial pressure fell significantly (P < 0.01) and to the same extent in the low-salt phases of the study. Clinic arterial pressure was consistently higher than 24 h ambulatory arterial pressure but the average changes induced by salt depletion were similar. The variability of 24 h ambulatory arterial pressure at constant salt intake was lower than that of clinic arterial pressure. However, the arterial pressure response to salt showed the same variability with the two methods. The reproducibility of the dichotomous classification of patients into salt-sensitive and -resistant was low both in terms of 24 h ambulatory and in terms of clinic blood pressure. CONCLUSION: Although on rechallenging the average arterial pressure response to salt remains unchanged in essential hypertensives, the individual responses are variable and the reproducibility of the dichotomous classification is unsatisfactory. The problem of dichotomizing patients into salt-sensitive and -resistant ones is only in very little part resolved by more precise arterial pressure estimates.
Zoccali et al. (Sun,) conducted a rct in mild essential hypertension (n=14). Low salt intake vs. High salt intake (170 mmol/day) was evaluated on Reproducibility of the arterial pressure response (intraclass correlation coefficient and K statistics). Short-term low salt intake significantly reduced arterial pressure (P<0.01), but individual responses were variable and the reproducibility of classifying patients as salt-sensitive or -resistant was low.