title: Monoamine oxidase--a inhibition reverses endothelial dysfunction in hypertensive rat aortic rings.
abstract: OBJECTIVE
  Monoamine oxidases (MAOs) are mitochondrial enzymes, with 2 isoforms, A and B that convert biogenic amines to their corresponding aldehydes via a reaction that produces hydrogen peroxide. Since MAO-A is the predominant form at vascular level we hypothesized that MAO-A-dependent H2O2 production may contribute to the development of endothelial dysfunction and, MAOs inhibition could improve the vascular function, respectively.
  
  
  METHODS
  To this aim aortic rings were isolated from female adult spontaneously hypertensive rats (SHR) and their corresponding (Wistar-Kyoto) controls. The effect of MAO-A inhibitor, clorgyline (10 micromol/l) on endothelium-dependent relaxation (EDR) in response to acetylcholine and endothelium-independent relaxation in response to sodium nitroprusside, was studied in isolated phenylephrine-preconstricted aortic segments in the presence of indometacine (10 micromol/l).
  
  
  RESULTS
  In hypertensive group EDR was significantly decreased - maximal relaxation (% of KCI, mean +/- SD) being 37 +/- 3.5 in SHR vs. 3.7 +/- 1.8 in controls. If experiments were done in the presence of clorgyline, EDR in control segments was unaffected. However, the compound restored normal EDR in aortic segments from hypertensive rats (maximal relaxation % of KCI, 13.7 +/- 2.3).
  
  
  CONCLUSIONS
  Inhibition of the MAO-A isoform might be useful in restoring endothelium-dependent relaxation in this experimental model of hypertension in rat.
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: A
authors: A
authors: Sturza
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: Silvia N
authors: SN
authors: Mirică
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: Oana
authors: O
authors: Duicu
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: Dorina
authors: D
authors: Gheorgheosu
authors: Department of Physiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: Lavinia
authors: L
authors: Noveanu
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: O
authors: O
authors: Fira-Mlădinescu
authors: Department of Pathophysiology, Faculty of Medicine, University of Medicine and Pharmacy Victor Babes, Timisoara.
authors: Danina M
authors: DM
authors: Muntean
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects*; D003010:Clorgyline / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000201:enzymology / Q000503:physiopathology; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D066298:In Vitro Techniques; D008955:Models, Cardiovascular; D008995:Monoamine Oxidase / Q000096:biosynthesis; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D008996:Monoamine Oxidase Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D008995:Monoamine Oxidase; D003010:Clorgyline; D000109:Acetylcholine