Our research investigates the role of angiotensin (Ang) II synthesis within the kidneys in hypertension. Past experiments have indicated that the intrarenal renin-angiotensin system (RAS) becomes activated during several forms of experimental and human hypertension. The importance of the RAS in the etiology of hypertension is underscored by the blood pressure-lowering effects of its pharmacological antagonists. Paradoxically, most hypertensive patients lack consistent signs of systemic RAS activation. This observation, and the recognition of RAS expressed within the kidney, serves as the basis for the suggestion that intrarenal RAS alterations underlie hypertension.
Renal angiotensinogen protein expression as determined by Immunohistochemistry in
Angiotensin II-infused mice vs. controls
(Am J Physiol Renal Physiol. 2008 Sep; 295(3): F772-9)
Changes in systolic BP (SBP, A) and body weight (B) of mice with ACE only
in the kidneys (ACE 9/9) in response to chronic angiotensin I infusion.