There was no change in plasma Ang II nor renalAT1R expression.32 Withoutthe protective arm of the RAAS, the net result is catastrophic as demonstratedin the salt-sensitive, Ang II-dependent hypertension model: the development ofmalignant hypertension associated to kidney damage.33 Inappropriate RAAS activation was related to increasedurinary angiotensinogen and intra-renal Ang II.33 This evidence concerns the gene AGT and substance dependence.