title: Aminopeptidase activity in renovascular hypertension.
abstract: BACKGROUND
  Renovascular hypertension is accompanied by increased renin-angiotensin system activity. Angiotensin II (Ang II) is degraded by aminopeptidases into various metabolites. Increased Ang II production and decreased Ang II degradation may have pathological consequences in maintaining high tissue/plasma Ang II levels.
  
  
  METHODS
  We report the effects of renovascular hypertension on alanyl- (AlaAP), arginyl- (ArgAP), cystinyl- (CysAP), aspartyl- (AspAP), glutamyl- (GluAP) and pyroglutamyl- (pGluAP) aminopeptidases, using arylamides as substrates. The enzymatic activities were analyzed in plasma, right atrium, lung, left ventricle and aortic ring of rats, normotensive (sham-operated) and hypertensive (Goldblatt two-kidney one-clip, G2K1C), treated or not with the AT1 receptor antagonist valsartan. All determinations were performed six weeks after surgery.
  
  
  RESULTS
  Whereas the atrium exhibited an increase, the lung, ventricle and aorta showed a decrease of aminopeptidases in G2K1C rats. Except in the aorta of normotensive rats, valsartan did not affect aminopeptidases in the groups studied.
  
  
  CONCLUSIONS
  The present study may imply reduced metabolism of angiotensin II in the lung and aorta of G2K1C rats. This down-regulation could prolong the half-life of Ang II and contribute to the maintenance of hypertension. Changes in AP activities did not appear to be part of the action mechanism of AT1 receptor blockade in hypertensive rats
authors.affiliation: Unit of Physiology, University of Jaén, Jaén, Spain.
authors.forename: Isabel
authors.initials: I
authors.lastname: Prieto
authors.forename: Francisco
authors.initials: F
authors.lastname: Hermoso
authors.forename: Marc
authors.initials: M
authors.lastname: de Gasparo
authors.forename: Félix
authors.initials: F
authors.lastname: Vargas
authors.forename: Francisco
authors.initials: F
authors.lastname: Alba
authors.forename: Ana B
authors.initials: AB
authors.lastname: Segarra
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Banegas
authors.forename: Manuel
authors.initials: M
authors.lastname: Ramírez
mesh_terms: D000626:Aminopeptidases / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001011:Aorta / Q000378:metabolism; D015536:Down-Regulation; D006325:Heart Atria / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism; D006973:Hypertension / Q000473:pathology; D006978:Hypertension, Renovascular / Q000201:enzymology*; D008168:Lung / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000378:metabolism; D013777:Tetrazoles / Q000494:pharmacology; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000068756:Valsartan
chemical_list: D000959:Antihypertensive Agents; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D013777:Tetrazoles; D000804:Angiotensin II; D000068756:Valsartan; D000626:Aminopeptidases; D014633:Valine