Abstract P129: Renal Necrotic Tissue Induces Hypertension

Abstract

The effect of renal necrotic tissue on blood pressure remain unclear. We hypothesized that infarcted renal tissue induces hypertension by stimulating inflammatory response. Partial renal infarction models were developed by ligating either upper branch (UL group) or lower branch (LL group) in the left renal artery. Mean arterial pressure (MAP) measured with telemetry quickly increased from 3 days after surgery, then gradually declined and reached a plateau within 7 days after surgery, which was 120.4±4.6 mmHg (increased by 23.8±2.5%) in UL group and 114.3±5.6 mmHg (increased by 19.0±1.1%) in LL group (n=8, p<0.01 vs baseline). Moreover, resection of the renal necrotic zone at day 14 th after ligation surgery normalized the MAP in partial renal infarction groups at day 28 th (UL+R: 121.1±5.9 to 98.3±5.1 mmHg; LL+R: 118.6±4.7 to 101.5±3.6 mmHg). The protein levels of TNFα and IL-6 in the left kidney homogenate significantly increased in UL group (11.5±3.4-fold; 3.8±1.2-fold) and LL group (8.4±2.7-fold; 2.7±0.83-fold) compared with the sham group at day 28 after ligation surgery (n=5, p<0.01 vs sham). Plasma concentration of TNFα and IL-6 also elevated in UL group (3.5±1.2-fold; 2.4±0.4-fold) and LL group (3.8±0.9-fold; 2.9±0.7-fold) at day 28 (n=7, p<0.01 vs sham). Inflammatory cell infiltration was significantly enhanced in UL (337±45 Inflammatory cells/HPF) and LL groups (314±27 Inflammatory cells/HPF) compared with sham group (22±14 Inflammatory cells/HPF) (n=7, p<0.01 vs sham). Moreover, resection of the renal necrotic zone at day 14 th after ligation surgery normalized the inflammatory response at day 28 th in UL+R and LL+R groups, compared with UL and LL groups. We concluded that renal necrotic tissue induces hypertension in C57BL/6 mice, possibly by stimulating of the inflammatory response.