Key result
Chronic NaCl exposure impairs working memory and disrupts circadian blood pressure regulation in salt-sensitive rats.
Why the study?
Elevated sodium intake links to hypertension and cognitive impairment, but whether trace drinking-water salinity impairs learning, memory, and blood-pressure regulation in salt-sensitive models was unknown.
Does trace sodium in drinking water impair memory and disrupt blood-pressure regulation in salt-sensitive rats?
Does trace sodium in drinking water impair memory and disrupt blood-pressure regulation in salt-sensitive rats?
p-value: p=<0.01
Chronic exposure to trace sodium concentrations in drinking water impairs working memory, elevates neuroinflammation, and disrupts autonomic blood-pressure rhythms in salt-sensitive rats.
Trace sodium impairs working memory in salt-sensitive models; leaves open human relevance for cognition and blood-pressure variability.
Trace sodium enters groundwater through saltwater intrusion and road-salt runoff. U.S. regions most affected also show disproportionately high rates of dementia and cardiovascular disease. Elevated sodium intake is linked to hypertension and mild cognitive impairment, particularly in salt-sensitive individuals. We therefore hypothesized that even trace increases in drinking-water salinity may impair learning and memory and disrupt blood-pressure regulation in a salt-sensitive model. Tap water from 28 U.S. cities was analyzed by flame photometry, revealing a range of 0.75-58.1 mg/L sodium, equivalent to 1.9-145.3 mg/L table salt (NaCl). Accordingly, adult male Dahl salt-sensitive (SS) rats (n=8/group; 4 wks old) received 0, 60, or 120 mg/L NaCl in Primo filtered water ad libitum for 32 weeks while maintained on 0.3% NaCl chow. At week 29, radiotelemetry probes were implanted; during weeks 31–32, rats were challenged with 2.0% NaCl chow for blood-pressure assessment. Body weight, food intake, and water intake were unchanged across groups. At week 30, Y-maze testing revealed significant working-memory impairment in the 120 mg/L group (ANOVA, p< 0.01) and a trend in the 60 mg/L group (p=0.1). Hippocampal IL-1β levels were elevated in both 60 and 120 mg/L groups, and IFN-γ was elevated in the 120 mg/L group (ANOVA, p< 0.05), suggesting increased neuroinflammation. Additionally, circadian blood-pressure regulation was disrupted in the 60 mg/L (p< 0.05) and 120 mg/L groups (p< 0.01). These findings indicate that chronic exposure to trace sodium concentrations, within the range observed in U.S. drinking water, can impair working memory, elevate neuroinflammation, and disrupt autonomic blood-pressure rhythms in salt-sensitive rats. Such effects parallel features of hypertension and mild cognitive impairment, suggesting that low-level salinity in drinking water may contribute to regional disparities in cardiometabolic and cognitive health and may warrant reconsideration of sodium guidelines. Funding support: R01HL152162, University of Toledo and University of South Florida Start-up Funds to Zubcevic This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
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Otmanowski et al. (2026) studied Salt sensitivity, memory impairment, and hypertension (n=24). Trace sodium (NaCl) in drinking water vs. 0 mg/L NaCl in drinking water was evaluated on Working-memory impairment (Y-maze testing) and circadian blood-pressure regulation (p=<0.01). Chronic exposure to 120 mg/L NaCl in drinking water significantly impaired working memory (p<0.01) and disrupted circadian blood-pressure regulation (p<0.01) in salt-sensitive rats.
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