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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 1and 2(controls) received tap water or 1% saline (salt) for 5 wk. Groups 3and 4received 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+.

Compared with age-matched men, women are resistant to the hypertensive effects of dietary NaCl; however, after menopause, the incidence of salt-sensitive hypertension is similar in women and men. We recently suggested that osmotically inactive Na+storage contributes to the development of salt-sensitive hypertension. The connective tissues, including those immediately below the skin that may serve as a reservoir for osmotically inactive Na+storage, are affected by menopause. We tested the hypothesis that ovariectomy (OVX) might reduce osmotically inactive Na+storage capacity in the body, particularly in the skin. Male, female-fertile, and female OVX Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet. The groups received the diet for 4 or 8 wk. At the end of the experiment, subgroups received 0.9% saline infusion and urinary Na+and K+excretion was measured. Wet and dry weight (DW), water content in the body and skin, total body Na+(rTBNa+) and skin Na+(rSKNa+) content were measured relative to DW by desiccation and dry ashing. There were no gender differences in osmotically inactive Na+storage in SD rats. All SD rats accumulated Na+if fed 8% NaCl, but rTBNa+was lower in OVX rats than in fertile rats on a low (P< 0.001)- and a high (P< 0.05)-salt diet. OVX decreased rSKNa+(P< 0.01) in the rats. A high-salt diet led to Na+accumulation (ΔSKNa+) in the skin in all SD rats. Osmotically inactive skin Na+accumulation was ∼66% of ΔSKNa+in female and 82% in male-fertile rats, but there was no osmotically inactive Na+accumulation in OVX rats fed 8% NaCl. We conclude that skin is an osmotically inactive Na+reservoir that accumulates Na+when dietary NaCl is excessive. OVX leads to an acquired reduction of osmotically inactive Na+storage in SD rats that predisposes the rats to volume excess despite a reduced Na+content relative to body weight.