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Abstract: FR-PO406

Low Cl- Diet Protects from Hypertension and Cardiac Hypertrophy After AngII Infusion in Mice Preserving Natriuresis

Session Information

  • Hypertension and CVD: Basic
    November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

  • 1601 Hypertension and CVD: Basic


  • Michea, Luis F., ICBM Facultad de Medicina, Universidad de Chile, Santiago, RM, Chile
  • Liberona, Jessica C., ICBM Facultad de Medicina, Universidad de Chile, Santiago, RM, Chile
  • Leon, Pablo Andres, ICBM Facultad de Medicina, Universidad de Chile, Santiago, RM, Chile

The increase of blood caused by Angiotensin II (AngII) depends on the expansion of vascular volume and the increase of total peripheral resistance. Besides acting as a vasoconstrictor, AngII increases renal Na+ reabsorption. Chloride is reabsorbed as the accompanying anion of Na+ and modulates natriuresis, and extracellular Cl- affects vascular smooth muscle cell contractility. We evaluated if low dietary Cl affected the pressor response to AngII infusion, cardiac hypertrophy, natriuresis, and vascular contractility.


C56BL/6J mice were allocated to 4 experimental groups: low-Cl diet (Cl replaced by HCO3, phosphate), normal-Cl diet (NaCl), AngII infusion (1.5 mg/Kg/day osmotic minipumps) or vehicle infusion (14 days). We measured systolic blood pressure (SBP) by the tail-cuff method. Natriuresis after a saline load (10% of body weight, i.p.) was assessed at baseline 4 and 14 days. Na+, K+ and Cl-excretion were measured (4 hours). We also measured cardiac hypertrophy and isotonic force development in aortic rings (high extracellular K+, phenylephrine) and NO-dependent relaxation.


In normal-Cl--diet mice, AngII infusion increased SBP from 103.3±9.1 mmHg to. 145.3±3.2 mmHg (n=6 per group, P<0.01 baseline vs. 14 days). In contrast, AngII infusion did not increase SBP in low-Cl diet mice (97.8±3.6 v/s 92.71±4.7 n=6 per group, n.s baseline vs. 14 days). Low Cl diet prevented cardiac hypertrophy after AngIi infusion (14 days). Normal Cl--diet mice presented hampered natriuretic response after AngII infusion (8.8±1.7 vs. 4.1±2.1 uEq/4h/g BW, baseline vs. 14 days respectively, P<0.01). Low- Cl--diet prevented the decrease in natriuresis after Ang II infusion (9.6±2.7 vs. 10.69±2.09 uEq/4h/g BW, baseline vs. 14 days respectively, P<0.01). AngII infusion increased the aortic rings maximal tension in response to phenylephrine, irrespective of dietary Cl. No changes in dose response to phenylephrine or Ach-induced NO-dependent vasodilation were observed among the groups.


Low Cl associated to a regular Na+ content in diet prevented the increase of blood pressure and cardiac hypertrophy in response to AngII infusion. The protective action of a low Cl- diet may be attributed to the protection of renal natriuretic response without affecting the vascular effects of AngII.


  • Government Support – Non-U.S.