Osmotically inactive skin Na+ storage involves a glycosaminoglycan cation exchange mechanism

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Internal sodium balance in DOCA-salt rats: a body composition study [Erratum in: Am J Physiol Renal Physiol. vol 290, pg F561-F562, 2006]

The idea that Na+ retention inevitably leads to water retention is compelling; however, were Na+ accumulation in part osmotically inactive, regulatory alternatives would be available. We speculated that in DOCA-salt rats Na+ accumulation is excessive relative to water. Forty female Sprague-Dawley rats were divided into four subgroups. Groups 1 and 2 (controls) received tap water or 1% saline (salt) for 5 wk. Groups 3 and 4 received subcutaneous DOCA pellets and tap water or salt. Na+, K +, and water were measured in skin, bone, muscle, and total body by desiccation and consecutive dry ashing. DOCA-salt led to total body Na + excess (0.255 ± 0.022 vs. 0.170 ± 0.010 mmol/g dry wt; P < 0.001), whereas water retention was only moderate (0.685 ± 0.119 vs. 0.648 ± 0.130 ml/g wet wt; P < 0.001). Muscle Na+ retention (0.220 ± 0.029 vs. 0.145 ± 0.021 mmol/g dry wt; P < 0.01) in DOCA-salt was compensated by muscle K+ loss, indicating osmotically neutral Na+/K+ exchange. Skin Na+ retention (0.267 ± 0.049 vs. 0.152 ± 0.014 mmol/g dry wt; P < 0.001) in DOCA-salt rats was not balanced by K+ loss, indicating osmotically inactive skin Na+ storage. We conclude that DOCA-salt leads to tissue Na+ excess relative to water. The relative Na + excess is achieved by two distinct mechanisms, namely, osmotically inactive Na+ storage and osmotically neutral Na+ retention balanced by K+ loss. This "internal Na+ escape" allows the maintenance of volume homeostasis despite increased total body Na+

Mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats

The idea that an osmotically inactive Na(+) storage pool exists that can be varied to accommodate states of Na(+) retention and/or Na(+) loss is controversial. We speculated that considerable amounts of osmotically inactive Na(+) are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na(+) reservoirs. Six week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 weeks. At sacrifice, we separated the tissues and determined their Na(+), K(+), and water content. Three weeks of growth reduced the total body Na(+) content relative to dry weight (rTBNa(+)) by 23%. This 'growth programmed' Na(+) loss originated mainly from the bone and the completely skinned and bone-removed carcasses. The Na(+) loss was osmotically inactive (45-50%), or osmotically active (50-55%). In rats aged 10 weeks, compared to HS, 4 weeks LS reduced rTBNa(+) by 9%. This dietary-induced Na(+) loss was osmotically inactive ( approximately 50%) and originated largely from the skin, while approximately 50% was osmotically active. LS for 1 week did not reduce skin Na(+) content. The mobilization of osmotically inactive skin Na(+) with long-term salt deprivation was associated with decreased negative charged skin glycosaminoglycan content and thereby a decreased water-free Na(+) binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies, but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis. Key words: extrarenal sodium balance, sodium reservoirs, glycosaminoglycans, hypertension, volume

The mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats.

The idea that an osmotically inactive Na(+) storage pool exists that can be varied to accommodate states of Na(+) retention and/or Na(+) loss is controversial. We speculated that considerable amounts of osmotically inactive Na(+) are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na(+) reservoirs. Six-week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 wk. At their death, we separated the tissues and determined their Na(+), K(+), and water content. Three weeks of growth reduced the total body Na(+) content relative to dry weight (rTBNa(+)) by 23%. This "growth-programmed" Na(+) loss originated from the bone and the completely skinned and bone-removed carcasses. The Na(+) loss was osmotically inactive (45-50%) or osmotically active (50-55%). In rats aged 10 wk, compared with HS, 4 wk of LS reduced rTBNa(+) by 9%. This dietary-induced Na(+) loss was osmotically inactive (pproximately 50%) and originated largely from the skin, while approximately 50% was osmotically active. LS for 1 wk did not reduce skin Na(+) content. The mobilization of osmotically inactive skin Na(+) with long-term salt deprivation was associated with decreased negatively charged skin glycosaminoglycan content and thereby a decreased water-free Na(+) binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis