| Summary: | Background: High salt intake has been associated with structural and functional vascular changes.1
Objective: To correlate urinary sodium excretion with endothelial function and arterial stiffness in non-diabetic hypertensive patients.
Methods: Cross-sectional study with non-diabetic hypertensive patients, both genders, aged 45–65 years, submitted to office blood pressure measurement, 24-hour urine sampling, carotid-femoral pulse wave velocity (PWV; Complior Analysis), central hemodynamic parameters by applanation tonometry (SphygmoCor) and microvascular reactivity by Laser Speckle Contrast Analysis (Pericam PSI)2.
Results: Patients (n = 18) were divided according to the urinary sodium excretion (UrNa) median: group 1 (UrNa <165mEq/24h) and group 2 (UrNa≥165mEq/24h). The mean age was 56 years, 72% were women. Although not statistically significant, group 2 presented higher systolic blood pressure (SBP, 136±12 vs 144±20 mmHg, p = 0.382) and diastolic blood pressure (84±10 vs 87±10 mmHg, p = 0.523). Serum insulin (11±5 vs 20±12 mcU/ml, p = 0.072), HOMA-IR (2.6±1.2 vs 4.9±3.0, p = 0.069), C-Reactive protein (CRP, 0.12±0.35 vs 0.78±0.83 mg/dL, p = 0.058) and PWV (8.8±2.1 vs 10.8±2.3 m/s, p = 0.093) were also higher in group 2. There were no significant differences in aortic SBP (127±16 vs 132±20 mmHg, p = 0.556), and in the peak of microvascular reactivity (95.5±24.0 vs 83.4±45.1, p = 0.505). Group 2 presented a higher proportion of patients with HOMA-IR greater than 2.7 (37.5 vs 70.0%, p = 0.047), CRP greater than 0.4 mg/dl (12.5 vs 55.6%; p = 0.064) and PWV greater than 10m/s (25 vs 80%, p = 0.020).
Conclusion: Although without significant differences in blood pressure and endothelial function, hypertensive patients with higher urinary sodium excretion showed changes suggestive of insulin resistance and arterial stiffness.
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