title: Renal perfusion in blacks: alterations caused by insuppressibility of intrarenal renin with salt.
abstract: We have reported that an increased intrarenal renin-angiotensin system activity may be responsible for the reduction in renal plasma flow (RPF) in apparently healthy blacks in comparison to healthy whites during high salt balance. To ascertain whether these differences only exist in the high salt state, we performed the following study, concentrating on the manipulation of the renin system during low salt intake. We measured in 19 healthy blacks and 22 healthy whites para-aminohippurate and inulin clearances as an indication of RPF and glomerular filtration rate, respectively, on both high (200 mmol/d) and low (10 mmol/d) salt balance in random order. A subset of 11 blacks and 12 whites additionally received an angiotensin II infusion while in low salt balance (3 ng/kg per minute for 45 minutes) and captopril to assess differences in RPF response to a converting enzyme inhibitor. The 19 whites had significantly higher RPF when compared with blacks (P=0.033) when studied on high salt. However, during low salt balance, the RPFs were comparable in the 2 groups. Plasma renin activity was similar in the 2 groups on both diets. In the subset that received angiotensin II and captopril while in low salt balance, the renal vascular response was not different in whites and blacks. These data provide additional support for the concept that the intrarenal tissue renin system is more active in blacks than whites on a typical (high salt) diet and that the difference reflects primarily incomplete tissue renin suppression with an increase in salt intake. The mechanism involved may contribute to the increased susceptibility to renal injury in blacks.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass, USA. daprice@partners.org
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Price
authors.forename: Naomi D L
authors.initials: ND
authors.lastname: Fisher
authors.forename: M Cecilia
authors.initials: MC
authors.lastname: Lansang
authors.forename: Radomir
authors.initials: R
authors.lastname: Stevanovic
authors.forename: Gordon H
authors.initials: GH
authors.lastname: Williams
authors.forename: Norman K
authors.initials: NK
authors.lastname: Hollenberg
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D044383:Black People; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism; D008297:Male; D011188:Potassium / Q000097:blood / Q000652:urine; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D012083:Renin / Q000187:drug effects / Q000378:metabolism; D012964:Sodium / Q000097:blood / Q000652:urine; D012982:Sodium, Dietary / Q000008:administration & dosage; D044465:White People
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D012982:Sodium, Dietary; D000804:Angiotensin II; D002216:Captopril; D012964:Sodium; D003404:Creatinine; D012083:Renin; D011188:Potassium
keywords: Non-programmatic