title: Glomerular permeability defect in hypertension is dependent on renin angiotensin system activation.
abstract: BACKGROUND
  The aim of the present study was to compare glomerular permeability alterations associated with experimental hypertension models known to have different effects on the circulating renin-angiotensin system (RAS).
  
  
  METHODS
  Five groups, 10 animals each, were studied. One group served as a nonhypertensive control. The other four groups of hypertensive animals were composed of spontaneously hypertensive rats, deoxycorticosterone acetate hypertensive rats, Goldblatt two-kidney, one-clip rats, and a group of Wistar rats infused with angiotensin II (200 ng/kg/min). Tail-cuff sphygmomanometric systolic blood pressure (BP), albumin permeability determined in isolated glomeruli exposed to oncotic gradients (P(alb)), glomerular filtration rate (GFR, iopamidol method), plasma renin activity (PRA), and albuminuria were evaluated.
  
  
  RESULTS
  Alterations in P(alb) and albumin excretion rate were more evident in the experimental models with an activation of the RAS despite similar levels of systolic BP and GFR. A positive correlation was found between P(alb) and albuminuria (r = 0.51; P < .001) and between systolic BP and albuminuria (r = 0.37; P < .01). No relation was found between systolic BP and P(alb).
  
  
  CONCLUSIONS
  The present study indicates that the activation of the RAS plays a significant role in the development of glomerular albumin permeability defects in hypertensive models and may contribute to the mechanisms that lead to target organ damage in hypertension.
authors.affiliation: Department of Medicina Clinica and Neurologia, University of Trieste, Trieste, Italy.
authors.forename: Riccardo
authors.initials: R
authors.lastname: Candido
authors.forename: Michele
authors.initials: M
authors.lastname: Carraro
authors.forename: Francesco
authors.initials: F
authors.lastname: Fior
authors.forename: Mary L
authors.initials: ML
authors.lastname: Artero
authors.forename: Cristina
authors.initials: C
authors.lastname: Zennaro
authors.forename: Louise M
authors.initials: LM
authors.lastname: Burrell
authors.forename: Belinda J
authors.initials: BJ
authors.lastname: Davis
authors.forename: Maria Rosa
authors.initials: MR
authors.lastname: Cattin
authors.forename: Moreno
authors.initials: M
authors.lastname: Bardelli
authors.forename: Luigi
authors.initials: L
authors.lastname: Faccini
authors.forename: Renzo
authors.initials: R
authors.lastname: Carretta
authors.forename: Bruno
authors.initials: B
authors.lastname: Fabris
mesh_terms: D000418:Albumins / Q000378:metabolism; D000804:Angiotensin II / Q000493:pharmacokinetics; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000502:physiology; D003900:Desoxycorticosterone / Q000031:analogs & derivatives / Q000633:toxicity; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism*; D008297:Male; D011863:Radioimmunoassay; D051381:Rats; D020303:Rats, Inbred Dahl; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000493:pharmacokinetics
chemical_list: D000418:Albumins; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D003900:Desoxycorticosterone; D012083:Renin