During Ang II infusion, circulating renin is suppressed but urinary renin is enhanced, highlighting the distinct responses of intrarenal and systemic origins of renin.11,12,14,20,21 Overactivation of intrarenal renin-angiotensin-system (RAS) contributes to pathogenesis of hypertension induced by Ang II infusion22–24 or inhibition of nitric oxide synthesis.25 We, therefore, determined urinary renin activity, active renin content, prorenin content, and total renin content at day 6 of treatment with control, Ang II, Ang II + PF, or Ang II + PF + sPRR-His. This evidence concerns the gene AGT and Hypertension.