The Impact of High Dietary Sodium on Cerebral Blood Flow Regulation

Abstract

High salt consumption is linked to increased stroke risk. In rodents, high dietary sodium has been shown to impair cerebral blood flow regulation. In humans, cerebrovascular reactivity to carbon dioxide (CO2) is a validated method for assessing the cerebrovasculature where a reduction in cerebrovascular reactivity is associated with cerebrovascular disease. Additionally, the ability for the brain to maintain cerebral blood flow despite changes in arterial blood pressure is termed cerebral autoregulation (CA). Dysfunctional CA is also predictive of strokes and all‐cause mortality. However, the effects of a high dietary sodium consumption on cerebrovascular reactivity and dynamic CA in healthy, young adults is unknown.PurposeWe tested the hypothesis that ten days of high dietary sodium feeding would impair cerebral blood flow regulation in healthy young adults.MethodsEight adults (6M/2F; age: 29 ± 11yrs; BMI: 26±3 kg/m2, Mean‐±SD) participated in a controlled feeding study that consisted of 10 days of either low‐ (LS: 1 g sodium/day), medium‐ (MS: 2.3 g sodium/day), or high‐sodium (HS: 7 g sodium/day) diets, in randomized order separated by at least a month. Urinary sodium excretion was determined to ensure compliance on diets. Transcranial Doppler of the right middle cerebral artery (MCA) velocity was assessed while participants lay supine. On the tenth day of the diet, cerebrovascular reactivity to high CO2 (via 8% CO2; hypercapnia) and low CO2 (via hyperventilation; hypocapnia) were assessed. Dynamic CA between spontaneous changes in mean arterial pressure to MCA velocity using a transfer function analysis was also measured. Data were analyzed using one‐way repeated measures ANOVA. Tukey post hoc comparisons were used when appropriate.ResultsUrinary sodium excretion (LS= 64±56, MS= 82±19, HS=250±213 mmol/24h, P=0.04) increased in a step‐wise manner. Brachial blood pressures were not different (systolic blood pressure= P=0.45; diastolic blood pressure: P=0.17). Cerebrovascular reactivity to hypercapnia (LS= 2.4±0.6, MS= 1.7±0.5, HS=2.5±0.7 %/mmHg, P=0.09) and to hypocapnia (LS= 1.8±0.6, MS= 1.9±0.6, HS=2.0±0.7 %/mmHg, P=0.72) were not different. Dynamic CA was also not different in the very low frequency (phase: LS= 71±23, MS= 72±38, HS=80±39°, P=0.69) and low frequency band (phase: LS= 42±14, MS= 45±11, HS=47±14°, P=0.62).ConclusionDespite the diets, these preliminary data suggest that high dietary sodium may not impair cerebral blood flow regulation in healthy young adults.Support or Funding InformationAcknowledgementsNIH Grant 1RO1HL128388