“…1 AH experimental models have showed biochemical and cardiovascular alterations. [2][3][4] Among the most common experimental models of AH in rats are genetic hypertension developed by Okamoto and Aoki 5 with the spontaneous hypertension model, Dahl salt-susceptible, a result of a defect in renal excrete sodium, neurogenic hypertension, defined as a permanent increase in blood pressure resulting from a fundamentally neural (central or peripheral) change. Renal hypertension may be renoprive, produced by severe reduction in renal function, renovascular hypertension that is due to partial obstruction of blood flow to the kidneys, or in some cases both.…”