title: L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension.
abstract: BACKGROUND
  We investigated whether the substrate for nitric oxide synthesis L-arginine is able to modify hypertension and left ventricular hypertrophy development induced by chronic blockade of nitric oxide synthase activity by NG-nitro-L-arginine-methyl ester (L-NAME).
  
  
  METHODS
  Four groups of rats were investigated: control, L-arginine 1.5 g kg-1, L-NAME 40 mg kg-1, and L-NAME +L-arginine in corresponding doses. Systolic blood pressure was measured by non-invasive tail-cuff plethysmography each week. After 4 weeks, the animals were sacrificed and hydroxyproline and coenzyme Q9 and Q10 concentrations in the left ventricle, and nitric oxide synthase activity in the left ventricle, kidney and brain were investigated.
  
  
  RESULTS
  In the L-NAME group, nitric oxide synthase activity was decreased in the left ventricle, kidney and brain, and hypertension, left ventricular hypertrophy and fibrosis developed. Heart remodelling was associated with the decrease of coenzyme Q9 and Q10 concentrations in the left ventricle. Simultaneous treatment with L-NAME and L-arginine prevented nitric oxide synthase activity diminution in the left ventricle but not in the kidney and brain, and completely failed to prevent hypertension, left ventricular hypertrophy and fibrosis. Nevertheless, l-arginine prevented the diminution of coenzyme Q9 and Q10 concentrations in the left ventricle.
  
  
  CONCLUSIONS
  We conclude that L-arginine failed to prevent hypertension, left ventricular hypertrophy and fibrosis development despite restoration of nitric oxide synthase activity in the left ventricle. However, L-arginine prevented the diminution of coenzyme Q levels in the left ventricle.
authors.affiliation: Department of Pathophysiology, Slovak Academy of Sciences, Bratislava, Slovak Republic. fedor.simko@fmed.uniba.sk
authors.forename: F
authors.initials: F
authors.lastname: Simko
authors.forename: I
authors.initials: I
authors.lastname: Luptak
authors.forename: J
authors.initials: J
authors.lastname: Matuskova
authors.forename: K
authors.initials: K
authors.lastname: Krajcirovicova
authors.forename: Z
authors.initials: Z
authors.lastname: Sumbalova
authors.forename: J
authors.initials: J
authors.lastname: Kucharska
authors.forename: A
authors.initials: A
authors.lastname: Gvozdjakova
authors.forename: J
authors.initials: J
authors.lastname: Simko
authors.forename: P
authors.initials: P
authors.lastname: Babal
authors.forename: O
authors.initials: O
authors.lastname: Pechanova
authors.forename: I
authors.initials: I
authors.lastname: Bernatova
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents; D001120:Arginine / Q000494:pharmacology*; D001921:Brain / Q000473:pathology; D006909:Hydroxyproline / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced* / Q000473:pathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology*; D007668:Kidney / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D051381:Rats; D017208:Rats, Wistar; D014451:Ubiquinone / Q000378:metabolism
chemical_list: D000959:Antihypertensive Agents; D014451:Ubiquinone; D001120:Arginine; D019001:Nitric Oxide Synthase; D006909:Hydroxyproline; D019331:NG-Nitroarginine Methyl Ester