Dahl salt-resistant rats are protected against angiotensin II-induced hypertension.

Angiotensin II is a potent endogenous vasoconstrictor that induces oxidative stress in hypertensive rodent models. Dahl salt-resistant (SR) rats are protected against hypertension after high salt or high fructose intake. However, whether these rats are also protected against angiotensin II-mediated hypertension has not been investigated. Dahl salt-sensitive (SS) and SR rats were infused with angiotensin II (10 or 50 ng/kg/min) or vehicle via a mini-osmotic pump for 2 weeks. Blood pressure was measured using the tail-cuff method. Paraffin sections of the thoracic aortas and kidneys were stained using hematoxylin/eosin or Masson trichrome. Renal gene expression was measured using reverse transcription-quantitative polymerase chain reaction. Angiotensin II (50 ng/kg/min) induced hypertension in SS rats, but not in SR rats, although low doses of angiotensin II (10 ng/kg/min) transiently increased blood pressure in SS rats. Angiotensin II (50 ng/kg/min) did not induce morphological changes in the aortic walls or kidneys. Angiotensin II (50 ng/kg/min) induced the expression of At1rb, Nox2, Il-17ra, Il-23r, Tgf-β, Il-1β and Il-6 in SS rats, but not in SR rats. In conclusion, SR rats were protected against angiotensin II-induced hypertension. This result implies that the genetic trait that determines salt sensitivity may also determine susceptibility to hypertension in response to vasoconstrictors.