Inflammation is considered as a major effector of arterial damage brought about by salt excess in animal models. In a randomized, single masked, cross-over study in 32 uncomplicated essential hypertensive patients, we assessed the effect of a short-term low-salt diet on biomarkers of innate immunity [procalcitonin (PCT), interleukin-6, C-reactive protein, and tumor necrosis factor-α (TNF-α)], adiponectin (ADPN, an anti-inflammatory cytokine), and leptin.
Patients were randomized to either a 10–20 mmol sodium diet and sodium tablets (180 mEq/day) to achieve a 200 mmol intake per day or the same diet and identical placebo tablets, each for 2 weeks. At the end of each of these periods, all patients underwent a 24-h urine collection, a fasting blood sampling, and a 24 h ambulatory blood pressure monitoring.
In parallel with expected increase in plasma renin activity and aldosterone (P <0.001), both PCT (+33%) and TNF-α (9%) rose at low salt intake (P ≤0.007) while ADPN underwent an opposite change (− 17%, P <0.001). In a linear regression analysis for repeated measurements, PCT was significantly and inversely related to urinary salt (weighted r = −0.27, P = 0.03). Changes in inflammation biomarkers did not differ in salt-sensitive (n = 7) and salt-resistant (n = 25) patients.
In essential hypertensive patients, a very low salt diet generates a pro-inflammatory phenotype characterized by an increase in PCT and TNF-α and an opposite effect on an anti-inflammatory cytokine like ADPN.