OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
RCT Entities:
OBJECTIVES: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 hypertensivepatients, 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. METHODS: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. RESULTS: 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. CONCLUSION: In essential hypertensivepatients, 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.
Authors: H Yavuzer; M Cengiz; S Yavuzer; M Rıza Altıparmak; B Korkmazer; H Balci; A L Yaldıran; H Uzun Journal: J Hum Hypertens Date: 2015-06-04 Impact factor: 3.012
Authors: Eliane Fe Wenstedt; Sanne Gs Verberk; Jeffrey Kroon; Annette E Neele; Jeroen Baardman; Nike Claessen; Özge T Pasaoglu; Emma Rademaker; Esmee M Schrooten; Rosa D Wouda; Menno Pj de Winther; Jan Aten; Liffert Vogt; Jan Van den Bossche Journal: JCI Insight Date: 2019-11-01
Authors: Stephen P Juraschek; Lara C Kovell; Lawrence J Appel; Edgar R Miller; Frank M Sacks; Alex R Chang; Robert H Christenson; Heather Rebuck; Kenneth J Mukamal Journal: J Am Coll Cardiol Date: 2021-06-01 Impact factor: 27.203
Authors: Liping Huang; Kathy Trieu; Sohei Yoshimura; Bruce Neal; Mark Woodward; Norm R C Campbell; Qiang Li; Daniel T Lackland; Alexander A Leung; Cheryl A M Anderson; Graham A MacGregor; Feng J He Journal: BMJ Date: 2020-02-24