Acute effects of salt on blood pressure are mediated by serum osmolality

Abstract

It is classically thought that it is the amount of salt that is critical for driving acute blood pressure responses. However, recent studies suggest that blood pressure responses, at least acutely, may relate to changes in serum osmolality. Here, we test the hypothesis that acute blood pressure responses to salt can be altered by concomitant water loading. Ten healthy patients free of any disease and medication underwent 4 interventions each a week apart in which they took 300 mL of lentil soup with no salt (visit 1), lentil soup with 3 g salt (visit 2), or lentil soup with 3 g salt and 500 mL water (visit 3) or 750 mL water (visit 4). At each visit, hourly blood measurements and blood pressure measurements (baseline, 1st, 2nd, 3rd, and 4th hour) were performed and plasma osmolarity, sodium and copeptin levels were measured. Patients receiving the 3 g salt showed a 6 mOsm/L change in osmolality with a 2.5 mmol/L change in plasma sodium and 10 mm Hg rise in systolic blood pressure at 2 hours. When the same patients drank salty soup with water, the changes in plasma osmolarity, plasma sodium, and blood pressure were prevented. The ability to raise blood pressure acutely with salt appears dependent on changes in plasma osmolality rather than the amount of salt. Our findings suggest that concurrent intake of water must be considered when evaluating the role of salt in blood pressure.

Relationship between water and salt intake, osmolality, vasopressin, and aldosterone in the regulation of blood pressure

“…The study of Kanbay and Coll reports an increase in BP in all the evaluated groups in the first 2 hours after the starting of the different protocols, but this difference remained significant at 3 and 4 hours only in the group that received the lentil soup with 3 g of salt. This group showed a similar pattern of changes even in plasma osmolality, sodium, and copeptin during the visits.…”

“…The study of Kanbay and Coll did not consider the aldosterone values and its effector mechanisms that are involved in the regulation of BP and volume. Salt intake and RAAS activation are regulated in an inverse fashion.…”

“…Kanbay and Coll . have reported a study showing that the acute effect of salt supplementation on blood pressure (BP) increase is dependent on plasma osmolality and that can be partially prevented by coadministration of water.…”

Hyperosmolality, High Blood Pressure, and Decreased Estimated Glomerular Filtration Rate in US Adolescents, National Health and Nutrition Examination Survey 1999–2012

“…Of note, epidemics of CKD with some features similar to MeN have been described in other warm climates, such as Sri Lanka [43]. Perhaps the most suggestive evidence that dietary sodium increases blood pressure through its effects on serum osmolality comes from a small but carefully executed study by Kanbay et al [44]. After drinking lentil soup with 3 g of added salt, the 10 volunteers had a mean increase in SBP of 10 mm Hg 2 h later, along with an increase in serum osmolality of 6 mOsm/kg.…”

On blood pressure effect of acute osmolar load

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We have read with great interest the insightful paper by Dr Kanbay et al, in the recent (Oct 2018 issue) issue of the Journal. 1 The paper highlights the inherent difficulty to separate the effect of serum sodium and serum osmolality, as they are fundamentally linked. While the escorting Commentary 2 primarily focused on potential interactions with renin-angiotensin-aldosterone system, a few other issues are worth mentioning.First, gastrointestinal intake of salt may elicit a different neurohormonal regulatory process than intravenous administration, which may offer an alternative interpretation for these experiments.Meanwhile, the debate in the current era is focused on "sodium," and it conveniently ignores the escalating use of sodium bicarbonate supplementation for correcting metabolic acidosis in chronic kidney disease patients, a population heavily impacted by comorbid hypertension.

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