The intrarenal angiotensin system and inflammation in Dahl salt‐sensitive hypertension

Abstract

Dahl salt‐sensitive (S) hypertension is characterized by renal damage, renal immune cell infiltration and low plasma renin activity. Recent studies have shown that the intrarenal angiotensin (ANGII) system may be activated in these rats and along with the immune system may play important roles in the development of renal injury and hypertension. However, the roles of intrarenal ANGII/immune systems in the Dahl salt‐sensitive hypertension are not clear. Dahl S rats were equipped arterial catheters and subjected to a 5‐week diet of high Na (8% NaCl) or high Na+ARB (ANGII AT1 receptor blocker, candesartan cilexetil, 15 mg/kg/day). By the end of week 5 in the high Na+ARB group: mean arterial pressure (MAP) was 145 ± 1 mmHg compared to the high Na group value of 168 ± 7 mmHg*; kidney tissue ANGII concentration, macrophages, TNFα, and MCP‐1 and urinary protein excretion were 3.2 ± 1.4 pg/mg, 7.1 ± 0.6 cells/mm2, 0.38 ± 0.01 pg/mg, 21.7 ± 1.4 pg/mg, and 168 ± 20 mg/day in ARB rats compared to the high Na rat values of 5.5 ± 0.7 pg/mg*, 22 ± 1.6 cells/mm2*, 0.52 ± 0.02 pg/mg*, 26.7 ± 1.5 pg/mg*, and 318 ± 43 mg/day*, respectively. In summary, long term ARB treatment in high Na Dahl S rats decreased renal tissue ANGII, renal inflammation, renal damage and MAP. The intrarenal angiotensin system plays an important proinflammatory role in the kidneys of Dahl S rats leading to renal damage and increased blood pressure. Support: NIH grant HL51971.