title: Angiotensin I-converting enzyme gene polymorphism influences chronic hypertensive response in the rat Goldblatt model.
abstract: OBJECTIVE
  In humans, the insertion/deletion polymorphism in the angiotensin (Ang) I converting enzyme (ACE) gene significantly determines ACE activity. The deletion allele induces higher ACE levels and is associated with hypertension in men. In the rat, a microsatellite marker in the ACE gene allows differentiation of the ACE alleles among strains with different ACE levels. We evaluated the effect of genetically determined ACE expression on the development of renovascular hypertension in the rat.
  
  
  RESULTS
  Systolic BP (SBP), ACE and angiotensin II (Ang II) levels were measured using the Goldblatt (Gb) model (two kidneys, one clip) in homozygous males of two inbred strains (F2) of Lewis x Brown-Norway (BN) rats. SBP was significantly higher in the BN-Gb rats compared to the Lewis-Gb rats throughout the study (F = 239.6, P < 0.001). An interaction was observed between SBP and strain (F = 2.92, P < 0.01). Plasma ACE activity was 100% higher in the BN-Gb than in the Lewis-Gb rats (P < 0.05). Ang II plasma levels were higher in the BN-sham than in the Lewis-sham rats (255 +/- 22 versus 161 +/- 16 pg/ml, P < 0.05), increased in both Gb groups and correlated significantly with SBP (r = 0.58, P < 0.01).
  
  
  CONCLUSIONS
  Genetically determined ACE expression in male rats enhances the chronic hypertensive response after the induction of renovascular hypertension. A relationship between circulating Ang II and the development of hypertension was also observed in this experimental model of genetically modulated hypertension.
authors.affiliation: Department of Cardiovascular Diseases, Medical School, P. Catholic University of Chile.
authors.forename: María P
authors.initials: MP
authors.lastname: Ocaranza
authors.forename: Ana M
authors.initials: AM
authors.lastname: Piddo
authors.forename: Perla
authors.initials: P
authors.lastname: Faúndez
authors.forename: Sergio
authors.initials: S
authors.lastname: Lavandero
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Jalil
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D002908:Chronic Disease; D005260:Female; D006978:Hypertension, Renovascular / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D009994:Osmolar Concentration; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D051381:Rats; D011914:Rats, Inbred BN; D011917:Rats, Inbred Lew; D012083:Renin / Q000097:blood; D013045:Species Specificity; D013599:Systole; D016277:Ventricular Function, Left
chemical_list: D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; D012083:Renin