Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow

Abstract

The American Heart Association recommends no more than 1500 mg of sodium/day as ideal. Some cohort studies suggest low-sodium intake is associated with increased cardiovascular mortality. Extremely low-sodium diets (≤500 mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow. The effects of an American Heart Association-recommended diet on sympathetic regulation of the vasculature are unclear. Therefore, we assessed whether a 1000 mg/d diet alters sympathetic outflow and sympathetic vascular transduction compared with the more commonly recommended 2300 mg/d. We hypothesized that sodium reduction from 2300 to 1000 mg/d would not affect resting sympathetic outflow but would reduce sympathetic transduction in healthy young adults. Seventeen participants (age: 26±2 years, 9F/8M) completed 10-day 2300 and 1000 mg/d sodium diets in this randomized controlled feeding study (crossover). We measured resting renin activity, angiotensin II, aldosterone, blood pressure, muscle sympathetic nerve activity, and norepinephrine. We quantified beat-by-beat changes in mean arterial pressure and leg vascular conductance (femoral artery ultrasound) following spontaneous sympathetic bursts to assess sympathetic vascular transduction. Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P<0.01 for all) but did not alter mean arterial pressure (78±2 versus 77±2 mm Hg, P=0.56), muscle sympathetic nerve activity (13.9±1.3 versus 13.9±0.8 bursts/min, P=0.98), or plasma/urine norepinephrine. Sympathetic vascular transduction decreased ( P<0.01). These data suggest that reducing sodium from 2300 to 1000 mg/d stimulates the renin-angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults.

Keywords: aldosterone; angiotensins; blood pressure; hypertension; renin.

Figure 1.

Effect of reduction in dietary sodium from 2300 mg/d to 1000 mg/d on renin angiotensin aldosterone system (RAAS) activation. Reducing dietary sodium from 2300 mg/d to 1000 mg/d in dietary sodium resulted in increased A) plasma renin activity (n=17), B) Aldosterone, (n=17) and C) Angiotensin II (n=14). Open bars denote the 2300 mg/day diet and filled bars denote the 1000 mg/day diet. *p<0.05.

Figure 2.

Effect of reduction in dietary sodium from 2300 mg/d to 1000 mg/d on resting sympathetic outflow. Representative tracings of electrocardiogram (ECG), muscle sympathetic nerve activity (MSNA), and blood pressure (BP) from one participant following A) 2300 mg/day and B) 1000 mg/day diets. Effect of reduction in dietary sodium from 2300 mg/d to 1000mg/d in dietary sodium resulted on C) burst frequency (n=11), D) burst incidence (n=11), and E) plasma norepinephrine (NE; n=17). Values of the measures were not different between diets (p>0.05 for all).

Figure 3.

Effect of reduction in dietary sodium from 2300 mg/d to 1000 mg/d on resting sympathetic vascular transduction. Effect of bursts of spontaneous muscle sympathetic nerve activity (MSNA) on A) increases in mean arterial pressure (MAP; n=11) and B) percent change in leg vascular conductance (LVC; n=8) over the 10 cardiac cycles following bursts of MSNA. A reduction in dietary sodium from 2300 mg/d to 1000 mg/d attenuated changes in MAP and LVC following spontaneous bursts of MSNA. Open squares denote the 2300 mg/day diet and closed circles denote the 1000 mg/day diet. *p<0.05.