High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans

Jennifer J. DuPonta, Jody L. Greaneya, Megan M. Wennerc, Shannon L. LennonEdwardsa, Paul W. Sandersf, William B. Farquhara, and David G. Edwards
Journal of Hypertension. Impact factor: 4.021

LOGO

Introduction Prevalence of CVD

39,8% (58.630)

An estimated 17.3 million people died from CVDs in 2008.

(New York States Department of Health, 2008)

Over 80% of CVD deaths take place in low- and middleincome countries.
2030 23 million people will die annually from CVDs.
(WHO, 2013)

The beneficial effects of dietary salt reduction on endothelial function could not be separated from the effects of decreases in BP The deleterious effects of excess salt consumption in humans are attributed to increase in BP (Law et al, 1991; Elliot et
al, 1996; Midgley et al, 1996)

Habitual low salt intake is associated with increased EDD in middle-aged and older adults with elevated SBP (Jablonski
et al, 2009)

Introduction
Experimental studies in animal: Dietary salt loading impaired cardiac, renal, and vascular function independent of arterial pressure in hypertensive and normotensive rats
(Frolich et al, 1993; Yu et al, 1998; Matavelli et al, 2007)

Excess salt intake effects independent of BP change

EDD (endothelium-dependent dilation), assesed by brachial artery flow-mediated dilation (FMD) improves in overweight and obese normotensive adults
(Dickinson et al, 2009)

Vascular endothelial dysfunction during salt loading independent of change in BP (Boegehold et al,

1995; Lenda et al, 2000; Lenda et al, 2002; Nurkiewicz et al, 2007; Zhu et al, 2007)

In normotensive rats fed up high-salt diet, skeletal muscle arteriolar responsiveness to endotheliumdependent stimulation reduced in the absence of change in BP
(Lenda et al, 2000; Lenda et al, 2002; Nurkiewicz et al, 2007)

Acute local infusion of hypertonic saline impairs cutaneous microvascular function in healthy normotensive individuals
(Dupont et al, 2011)

Objective

To demonstrate that the effects of dietary sodium on vascular function are independent of BP in normotensive humans

Methods
Participant Inclusion criteria: - 14 healthy salt-resistant individuals - 22 to 46 years Exclusion criteria: - History of HT - DM - CVD - Renal impairment - Malignancy - Menopausal women - Tobacco use - Obese (BMI>30 kg/m2) 37-day run-in diet (100 mmol sodium/day) 7 days low-sodium diet (20 mmol/day) 7 days high-sodium diet (300350 mmol/day) Dietary potassium intake averaged 70.9+3.7 mmol/day carbohydrates 50%, fat 30%, protein 20%

Dietary salt perturbation

Methods
Collected during the last 24-hr period of the low-sodium and high-sodium conditions 24-hr BP BP were measured every 20 min (awake) and every 30 min (sleep) Laboratory BP during the low-sodium and high-sodium testing visits to the laboratory

24-hr urine and BP

Salt resistance

5 mmHg or less change in 24-hr MAP while on the low-sodium and the highsodium diets >5 mmHg excluded

Methods
Assessment of EDD
Patient was supine, right arm supported at heart level

BP cuff was placed on the proximal forearm 3 cm below the antecubitalcrease

Baseline image recording

the cuff was rapidly inflated to 200mmHg for 5 min

Image and blood velocity recording

Methods
Assessment of EID Blood Analysis

5 participants Administration of NTG 0.4 mg Image recording baseline and 10 min after NTG administration

Venous blood sample was used to measure hemoglobin, hematocrit, plasma osmolality, PRA, serum aldosteron, serum angiotensin II

Statistical Analysis

Two-tailed, paired t-tests Significance at p < 0.05

Result

Result Dietary salt perturbation

Result
Dietary salt perturbation

Result
Dietary salt perturbation

Result

Vascular function

Shear rate AUC did not differ between low-sodium and high-sodium diets (182805455 vs184096216; P>0.05)

EID (% diameter)

Discussion