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Tissue sodium excess is not hypertonic and reflects extracellular volume expansion.

ABSTRACT: Our understanding of Na⁺ homeostasis has recently been reshaped by the notion of skin as a depot for Na⁺ accumulation in multiple cardiovascular diseases and risk factors. The proposed water-independent nature of tissue Na⁺ could induce local pathogenic changes, but lacks firm demonstration. Here, we show that tissue Na⁺ excess upon high Na⁺ intake is a systemic, rather than skin-specific, phenomenon reflecting architectural changes, i.e. a shift in the extracellular-to-intracellular compartments, due to a reduction of the intracellular or accumulation of water-paralleled Na⁺ in the extracellular space. We also demonstrate that this accumulation is unlikely to justify the observed development of experimental hypertension if it were water-independent. Finally, we show that this isotonic skin Na⁺ excess, reflecting subclinical oedema, occurs in hypertensive patients and in association with aging. The implications of our findings, questioning previous assumptions but also reinforcing the importance of tissue Na⁺ excess, are both mechanistic and clinical.

SUBMITTER: Rossitto G

PROVIDER: S-EPMC7445299 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Tissue sodium excess is not hypertonic and reflects extracellular volume expansion.

Rossitto Giacomo G Mary Sheon S Chen Jun Yu JY Boder Philipp P Chew Khai Syuen KS Neves Karla B KB Alves Rheure L RL Montezano Augusto C AC Welsh Paul P Petrie Mark C MC Graham Delyth D Touyz Rhian M RM Delles Christian C

Nature communications 20200824 1

Our understanding of Na+ homeostasis has recently been reshaped by the notion of skin as a depot for Na+ accumulation in multiple cardiovascular diseases and risk factors. The proposed water-independent nature of tissue Na+ could induce local pathogenic changes, but lacks firm demonstration. Here, we show that tissue Na+ excess upon high Na+ intake is a systemic, rather than skin-specific, phenomenon reflecting architectural changes, i.e. a ...[more]

PMID: 32839436

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Project description:The renal distal nephron plays an important role in the maintenance of sodium balance, extra cellular volume and blood pressure. The degree of water transport, via aquaporin2 water channels (AQP2), and sodium transport, via epithelial sodium channels (ENaC) in renal collecting duct principal cells are reflected by the level of urinary excretion of AQP2 (u-AQP2) and the ?-fraction of ENaC (u-ENaC?). The effects of an acute intravenous volume load with isotonic saline, hypertonic saline and glucose on u-AQP2, u-ENaC? and underlying mechanisms have never been studied in a randomized, placebo-controlled trial in healthy humans.We studied the effects of 0.9% saline (23 ml/kg), 3% saline (7 ml/kg) and 5% glucose (23 ml/kg) on u-AQP2 and u-ENaC?, fractional sodium excretion (FENa), free water clearance (CH2O), and plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (ANG II) and aldosterone (Aldo) in a randomized, crossover study of 23 healthy subjects, who consumed a standardized diet, regarding calories, sodium and fluid for 4 days before each examination day.After isotonic saline infusion, u-AQP2 increased (27%). CH2O and u-ENaC? were unchanged, whereas FENa increased (123%). After hypertonic saline infusion, there was an increase in u-AQP2 (25%), u-ENaC? (19%) and FENa (96%), whereas CH2O decreased (-153%). After isotonic glucose infusion, there was a decrease in u-AQP2 (-16%), ENaC? (-10%) and FENa (-44%) whereas CH2O increased (164%). AVP remained unchanged after isotonic saline and glucose, but increased after hypertonic saline (139%). PRC, AngII and p-Aldo decreased after isotonic and hypertonic saline infusion, but not after glucose infusion.Volume expansion with 3% and 0.9% saline increased u-AQP2, while isotonic glucose decreased u-AQP2. Infusion of hypertonic saline increased u-ENaC?, whereas u-ENaC? was not significantly changed after isotonic saline and tended to decrease after glucose. Thus, the transport of water and sodium is changed both via the aquaporin 2 water channels and the epithelial sodium channels during all three types of volume expansion to regulate and maintain water- and sodium homeostasis in the body.Clinical Trial no: NCT01414088.

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Tissue sodium excess is not hypertonic and reflects extracellular volume expansion.

Publications

Tissue sodium excess is not hypertonic and reflects extracellular volume expansion.

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