Abstract

To the Editor: Sodium-dependent mechanisms play a role in the pathogenesis of hypertension. He et al recently demonstrated that in normotensive and hypertensive subjects an acute reduction in salt intake, from 350 to 10 mmol/d for 5 days, was associated with a decline in serum sodium by ≈3 mmol/L.1 Conversely, a progressive increase in salt intake from 10 to 250 mmol/d by a daily amount of 50 mmol caused an increase in serum sodium in normotensive subjects, but not hypertensive patients.1 These investigators speculated that small changes in serum sodium might directly affect the hypothalamic control of blood pressure through the local pituitary renin-angiotensin system.1 Ouabain is a steroid hormone, which is released from the hypothalamus and the adrenal gland. It is implicated in sodium homeostasis and exerts direct actions on the vasculature, the heart,2 and tubular sodium reabsorption.3 In individuals randomly recruited from a Flemish population, blood pressure increased by 2.2 mm Hg systolic and 1.4 mm Hg diastolic for each 50-mmol/d increment in urinary sodium excretion when the plasma ouabain concentration was below the median (140 pmol/L).4 No association between blood pressure and urinary sodium was found when plasma ouabain exceeded the …

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