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Abstract: SA-PO1097

Renin-Independent Blood Pressure Development in Dahl Salt-Sensitive Rats

Session Information

Category: Hypertension

  • 1102 Hypertension: Basic and Experimental - Renal Causes and Consequences


  • Ilatovskaya, Daria, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Levchenko, Vladislav, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Spires, Denisha R, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Pavlov, Tengis S., Henry Ford Health System, Detroit, Michigan, United States
  • Staruschenko, Alexander, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

RAAS is considered to be the central regulator of water and salt homeostasis; angiotensin receptors’ and/or ACE inhibitors are widely employed to control blood pressure (BP) in humans. Here we used renin knockout (Ren−/−) rats created on the Dahl Salt-Sensitive (SS) rat background to study renin-independent BP development; these rats exhibit polyuria, reduced weight and lower mean arterial pressure (MAP) compared to wild type controls.


To test the involvement of renin in the BP regulation of the Dahl SS rats, 9 week old Ren−/− rats and their wild type littermates were kept on 0.4% NaCl diet since weaning (normal salt, NS), and then challenged with sodium deficient (SD, 0.01%) or high salt (HS, 4% NaCl) diets for 11 days. BP was recorded via telemetry, and kidney function and tissue damage were assessed.


On NS diet Ren−/− rats have a significantly lower MAP compared to littermates (65.9 ± 2.1 vs 121.9 ± 1.9 mmHg). After a HS diet was introduced, we observed a very fast raise in MAP in the Ren−/− rats (ΔMAP was 60.4 ± 7.1 mmHg over a 5 day period, compared to 5 ± 0.4 mmHg in the littermates). In the Ren−/− group HS diet caused mortality within 8 days, which was not observed in the littermates. SD diet did not affect BP and survival rates in either group. 24 hr urinary output was increased in the wild type littermates on HS (not measured in the Ren−/− group due to mortality). However, in all SD diet fed groups urinary output was reduced (15.7 ± 1.7 vs 2.5 ± 0.2 ml/100g before diet switch, and 1.9 ± 0.7 vs 4.8 ± 0.9 ml/100g on SD diet (Ren−/− vs littermates)). On NS diet GFR was found to be lower in the Ren−/− rats (0.18 ± 0.03 ml/min/100g vs 0.54 ± 0.04 in littermates), and HS diet induced an increase in GFR in the littermates on day 10, whereas SD diet did not affect GFR in either group. No difference was found in electrolyte excretion between groups fed a SD diet. Histological analysis revealed exacerbated damage to the hearts and kidneys of the Ren−/− rats fed a SD diet compared to wild type littermates.


BP in the Ren−/− Dahl SS rat increases in response to salt intake, which suggests an involvement of the non-renin components in this mechanism; however, Ren−/− animals are able maintain homeostasis when challenged a SD diet. These data open new avenues to understanding the role of RAAS in SS hypertension.


  • NIDDK Support