The Journal of Clinical Hypertension | 2019
On blood pressure effect of acute osmolar load
Abstract
Dear Editors, 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 so‐ dium and serum osmolality, as they are fundamentally linked. While the escorting Commentary2 primarily focused on potential interac‐ tions with renin‐angiotensin‐aldosterone system, a few other issues are worth mentioning. First, gastrointestinal intake of salt may elicit a different neu‐ rohormonal regulatory process than intravenous administration, which may offer an alternative interpretation for these exper‐ iments.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. Second, for some time, it has been debated in clinical nephrology, whether injection of hypertonic saline (23% sodium chloride) during intra‐dialytic hypotension would confer symptomatic and blood pressure (BP) benefits beyond from what is expected for volume expansion.3,4 The Authors’ experiments1 certainly suggest so. Third, after weight‐reduction surgeries, the notably decrease in BP is almost immediate, coinciding with re‐ duction of dietary intake and even preceding the remarkable loss of body weight;5 the paper by Kanbay et al may provide at least a partial explanation for such observations. Fourth, the elevated copeptin levels are raising the question of relative contribution of elevated arginine vasopressin (antidiuretic hormone) levels to the BP response observed. And, finally, we shall remember that the achieved osmolar load will be partly dependent on the patients’ weight, but this was unknown for the patients of this current paper. Administration of sodium load is somewhat unique, as it is— unlikely, for example, urea—an effective osmole and does not pen‐ etrate intracellular (IC) compartment passively. Acute salt loading, even without water intake, should result in expansion of extracel‐ lular (EC) water space due to transcellular migration of H2O, along the osmolar gradient and may contribute to rise of EC water space. Interestingly, exact technology with bioimpedance spectroscopy is available to assess such changes of IC and EC water spaces.6 The logical counterpoints of these experiments may be to ex‐ amine the effect of equimolar administration of sodium chloride as hypertonic saline and intravenous mannitol to separate out the ef‐ fect of gastrointestinal absorption vs. exposure to osmotically active hyperosmolar solution, respectively. More than anything, this paper perhaps highlights how little we know. Respectfully submitted, The Authors ACKNOWLEDGMENTS