title: Angiotensin-(1-7)-induced renal vasodilation is reduced in human kidneys with renal artery stenosis.
abstract: BACKGROUND
  Angiotensin-(1-7) modulates renal blood flow in humans with essential hypertension by inducing vasodilation and counterbalancing angiotensin II-induced vasoconstriction. Little is, however, known about the effects of angiotensin-(1-7) in kidneys with atherosclerotic renal artery stenosis. We previously demonstrated that the effect of angiotensin-(1-7) is reduced in patients with increased activity of the renin-angiotensin system. As the renin-angiotensin system is also activated in kidneys with renal artery stenosis, we hypothesized that the vasodilatory effect of angiotensin-(1-7) is also reduced in such kidneys.
  
  
  METHODS
  Therefore, we selectively measured mean renal blood flow (¹³³Xenon washout method) before and during local infusion of angiotensin-(1-7) (0.27, 0.9, and 2.7 ng/kg per min) in hypertensive patients who were angiographically evaluated for the presence of renovascular abnormalities. Data were analyzed in three groups: stenotic kidneys, nonstenotic kidneys with renal artery stenosis of the contralateral kidney (contralateral stenotic kidneys), or essentially hypertensive controls without renovascular abnormalities (matched for urinary sodium excretion).
  
  
  RESULTS
  Angiotensin-(1-7) infusion resulted in an increase in renal blood flow in matched controls. In stenotic kidneys however, the effect of angiotensin-(1-7) was significantly reduced as compared to controls. The angiotensin-(1-7) effect in contralateral stenotic kidneys was comparable to controls.
  
  
  CONCLUSIONS
  Angiotensin-(1-7)-induced vasodilation is reduced in stenotic kidneys, but not in contralateral stenotic kidneys. This suggests that the altered blood flow regulation in kidneys with atherosclerotic renal artery stenosis is a local phenomenon and not related to generalized atherosclerotic burden. Probably, the renin-angiotensin system activation, bioavailability of nitric oxide, and structural changes in the stenotic kidney play a role in this phenomenon.
authors.affiliation: aDepartment of Internal Medicine bDepartment of Radiology, Maastricht University Medical Centre (MUMC+), Maastricht, The Netherlands.
authors.forename: Daan J L
authors.initials: DJ
authors.lastname: Van Twist
authors.forename: Alfons J H M
authors.initials: AJ
authors.lastname: Houben
authors.forename: Michiel W
authors.initials: MW
authors.lastname: De Haan
authors.forename: Guy J M
authors.initials: GJ
authors.lastname: Mostard
authors.forename: Peter W
authors.initials: PW
authors.lastname: De Leeuw
authors.forename: Abraham A
authors.initials: AA
authors.lastname: Kroon
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology*; D016022:Case-Control Studies; D000075222:Essential Hypertension; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000494:pharmacology*; D012077:Renal Artery / Q000187:drug effects; D012078:Renal Artery Obstruction / Q000503:physiopathology*; D012079:Renal Circulation; D012084:Renin-Angiotensin System / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D010446:Peptide Fragments; D000803:Angiotensin I; C118790:angiotensin I (1-7)