Key result
Dietary sodium intake and proximal tubular handling interact to affect blood pressure, with nighttime diastolic pressure 4.9 mm Hg higher in the lowest tertiles of both markers (P<0.001).
Why the study?
How do sodium dietary intake and renal sodium handling interact to affect blood pressure in untreated or washed-out subjects?
Observational (n=766)
How do sodium dietary intake and renal sodium handling interact to affect blood pressure in untreated or washed-out subjects?
Sodium dietary intake and proximal tubular handling interact to influence blood pressure, suggesting individual variations in renal sodium handling modulate the blood pressure response to dietary sodium.
Answers are grounded in this paper and cite their sources.
Suggests personalized sodium sensitivity; leaves open causal validation in prospective studies.
There is abundant evidence that sodium intake is related to blood pressure. However, the relationship varies between individuals and is probably determined by renal sodium handling. We investigated clinic and ambulatory blood pressure in relation to interactions between sodium dietary intake and renal handling, as assessed by 24-hour urinary sodium excretion and endogenous lithium clearance, respectively. We calculated fractional excretion of lithium and fractional distal reabsorption rate of sodium, as markers of proximal and distal sodium handling, respectively. The 766 subjects included 379 men and 478 ambulatory hypertensive patients. They were never treated (n=697) or did not take antihypertensive medication for ≥2 weeks (n=69). In adjusted analyses, none of the associations of urinary sodium excretion, fractional excretion of lithium, and fractional distal reabsorption rate of sodium with clinic or ambulatory blood pressure were statistically significant (P≥0.09). However, there was significant (P=0.01) interaction between urinary sodium excretion and fractional excretion of lithium in relation to nighttime diastolic blood pressure. In tertile 3 but not tertiles 1 and 2 of fractional excretion of lithium, nighttime diastolic pressure was positively associated with urinary sodium excretion (P=0.03). However, nighttime diastolic pressure was higher in tertile 1 than tertile 3 of fractional excretion of lithium (+2.0 mm Hg; P=0.01), especially in the bottom tertile of urinary sodium excretion (+4.9 mm Hg; P<0.001). Similar trends were observed for nighttime systolic pressure and clinic and 24-hour diastolic pressure. In conclusion, sodium dietary intake and proximal tubular handling interact to be associated with blood pressure.
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Zou et al. (2013) conducted an observational in Hypertension (n=766). Dietary sodium intake and renal sodium handling was evaluated on Clinic and ambulatory blood pressure (p=0.01). Dietary sodium intake and proximal tubular handling interact to affect blood pressure, with nighttime diastolic pressure 4.9 mm Hg higher in the lowest tertiles of both markers (P<0.001).
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