The role of plasma IL‐6 and IL‐10 during DOCA‐salt hypertension

Abstract

Interleukin‐10 (IL‐10) is an important immunoregulatory cytokine that inhibits the expression of pro‐inflammatory cytokines including interleukin‐6 (IL‐6), reduces vascular dysfunction and blood pressure in various animal models. Previous reports demonstrate an increase in plasma IL‐6 during different time periods of deoxycorticosterone acetate (DOCA) ‐salt hypertension and that increases in mean arterial pressure (MAP) are independent of plasma IL‐6. Reports also suggest that plasma IL‐10 is decreased during DOCA‐salt hypertension. We tested whether the reduction of plasma IL‐10 is dependent on increases in plasma IL‐6 and if plasma IL‐10 plays a role in attenuating DOCA‐salt hypertension. Ten to twelve week old IL‐6 knockout (KO) mice and their wild‐type (WT) controls were subjected to uninephrectomy and DOCA‐salt (1.5 mg/g) treatment for 3 weeks. Baseline MAP determined by radiotelemetry was not different between IL‐6 KO and WT mice (122 ± 2 and 129 ± 5 mmHg, respectively). The average MAP during days 16 – 20 of DOCA‐salt hypertension was similar between IL‐6 KO and WT mice (157 ± 7 and 162 ± 6 mmHg, respectively). Baseline plasma IL‐6 in WT mice was 43 ± 5 pg/mL and 96 ± 8 pg/mL on day 20 of DOCA‐salt hypertension. Baseline plasma IL‐10 was 80 ± 9 and 75 ± 10 pg/mL for WT and IL‐6 KO mice, respectively. DOCA‐salt hypertension significantly reduced plasma IL‐10 on day 20 to 2 ± 1 and 9 ± 3 pg/mL for WT and IL‐6 KO mice, respectively. Plasma levels of IL‐10 were significantly higher in IL‐6 KO mice when compared to WT controls. Our results suggest that reduction of plasma IL‐10 is independent of increases in plasma IL‐6 and plasma IL‐10 does not play a role in attenuating DOCA‐salt hypertension.