Interleukin‐1β upregulates components of the intra‐renal renin‐angiotensin system but does not induce salt‐sensitive hypertension.

Macrophage infiltration of the kidney is frequently observed in salt‐sensitive hypertension, but the role of these cells in blood pressure control is incompletely understood. We tested whether interleukin‐1β, a key pro‐inflammatory cytokine produced by macrophages, affects expression of components of the renin‐angiotensin system in the kidney, and whether chronic elevation of IL‐1β levels induces salt‐sensitive hypertension. Male C57BL/6 mice underwent 14‐day s.c. IL‐1β infusion (10ng/h), while maintained on either a normal (0.4% NaCl; n = 6) or high salt diet (4% NaCl; n = 6). Normal or high salt diet‐treated mice not undergoing IL‐1β infusion served as controls (n = 4 & 4). Quantitative real‐time PCR revealed that renal cortical expression of renin and angiotensinogen approximately doubled in both normal (2 −ΔΔCT = 2.3 ± 0.4 and 1.9 ± 0.4) and high‐salt treated mice receiving IL‐1β infusion (2 −ΔΔCT = 1.9 ± 0.5 and 1.9 ± 0.4) compared to non‐infused normal salt (2 −ΔΔCT = 1.1 ± 0.2 and 1.1 ± 0.2) and high salt‐treated mice (2 −ΔΔCT = 1.0 ± 0.1 and 1.1 ± 0.2; P Infusion < 0.05 for both genes). No significant difference in renal cortical angiotensin AT1a receptor expression was observed between groups. Systolic blood pressure (tail cuff plethysmography) at day 14 of IL‐1β infusion was not significantly different between normal (108 ± 5 mmHg) and high salt‐diet treated mice (105 ± 4 mmHg). Thus, despite increasing expression of key components of the renin‐angiotensin system, chronic elevation of IL‐1β does not induce salt‐sensitive hypertension.