The Impact of Dietary Sodium on Sympathetic and Blood Pressure Reactivity Assessed using the Cold Pressor Test

Abstract

High dietary sodium intake increases sympathetic and blood pressure (BP) reactivity in rodents, but it is not known if dietary sodium similarly affects reactivity in non‐hypertensive humans. Importantly, exaggerated sympathetic and BP responses are predictive of future hypertension risk.PURPOSEWe hypothesized that high dietary sodium would increase sympathetic and BP reactivity in male and female adults. The cold pressor test (CPT) was used to assess reactivity.METHODSTwenty‐seven healthy, non‐hypertensive adults (16M/11F; age: 26±7yrs; BMI: 24.7±1 kg/m2; mean±SD) participated in a controlled feeding study that consisted of 10 days of low (LS: 1.0 g/day), recommended (MS: 2.3 g/day), or high (HS: 7.0 g/day) sodium diets, in random order with at least a one‐month washout between diets. Twenty‐four hour urine samples were collected and sodium excretion was calculated to ensure compliance on the respective diets. Muscle sympathetic nerve activity (MSNA) was directly assessed using peroneal microneurography and beat‐to‐beat BP was assessed using photoplethysmography at rest and throughout the CPT. The CPT was completed by having participants immerse their dominant hand in an ice slurry (3° to 5°C) for 2 minutes. Data were analyzed using two‐way repeated measures ANOVAs.RESULTSAs expected, twenty‐four hour sodium excretion increased with increasing amounts of dietary salt (LS: 42±40, MS: 84±36, HS: 253±111 mmol/24 hours, main effect of diet, p<0.0001), with no apparent sex differences (p = 0.98). The CPT robustly increased MSNA, but there was no effect of diet (Δ MSNA burst frequency LS: 13±6, MS: 16±6, HS: 15±5 bursts/min, p = 0.23). Similarly, the CPT acutely increased systolic BP, but there was no effect of diet (Δ systolic BP LS: 18±11, MS: 20±12, HS: 18±11 mmHg, p = 0.44).CONCLUSIONThese data suggest that 10 days of high dietary salt intake does not affect MSNA or BP responses to the CPT in young, healthy, non‐hypertensive adults.Support or Funding InformationSupported by NIH Grant 1R01HL128388