Abstract P187: Partial Renal Infarction Induces Hypertension

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Renal infarction is an under-diagnosed and under-reported phenomenon. The U.S. incidence of renal infarction is estimated at 1.4%. Systemically thromboembolic originate from thrombus in the heart or aorta while renal infarction in situ typically involves the main renal artery or its branches. Acute or aggravated hypertension is commonly observed in previously normotensive or hypertensive patients with renal infarction. However, these pathophysiological mechanisms have not been elucidated. The goal of this study was to develop a hypertensive mouse model of renal infarction. Partial renal infarction was performed in C57BL/6 mice by ligating either the upper (LU) or lower (LL) branch of the renal artery in the left kidney while the right kidney remained intact. The mean arterial pressure (MAP) was continuously measured with a telemetry system in conscious mice fed 4 weeks of normal salt diet (NS) (0.4% NaCl) followed by 4 weeks of high salt diet (HS) (4% NaCl). Plasma renin concentration (PRC), renin mRNA in the kidney and TNF-α were measured. Body weight, salt and fluid intakes were similar in mice with LU and LL ligation compared with sham operated mice. The weight of the left kidney decreased by 16.3% in LU (118.1±8.9 mg) and 14.2% in LL (121.5±7.8 mg) compared with sham operated mice (141.0±9.5 mg) (n=6; p<0.05 vs sham). The right kidney weight increased by 41.5% in LU (201.3±15.6 mg) and 38.2% in LL (196.6±8.1 mg) compared with sham mice (142.2±8.8 mg) (n=6; p<0.01 vs sham). MAP in mice fed NS elevated by 25% in LU (119.4±12.9 mmHg) and 19.1% in LL (113.7±10.6 mmHg), compared with sham (95.4±4.7 mmHg) (n=4; p<0.05 vs sham). HS further increased the MAP to 124.2±17.4 mmHg in LU and 118.6±14.8 mmHg in LL mice. PRC decreased by 50.0% in LU (30.7±8.63 ng/ml) and 62.7% in LL (22.9±10.8 ng/ml), compared with sham operated mice (61.4±12.6 ng/ml) (n=6; p<0.05 vs sham). Expression of local renin mRNA in the left kidney was upregulated by 113.4% in LU and 64.1% in LL mice, compared with the sham. Inflammatory cytokines TNF-α was increased by 174.2% in LU and 106.3% in LL mice. In conclusion, we developed a mouse model of partial renal infarction with hypertension in C57BL/6 mice. The mechanism of hypertension may be due to the upregulation of local renin angiotensin system and inflammation.