title: Structure and function of the rat basilar artery during chronic nitric oxide synthase inhibition.
abstract: OBJECTIVE
  Nitric oxide is an important regulator of vascular tone and may also be implicated in the modulation of vascular growth and structure. This study presents the effects of chronic nitric oxide inhibition, with or without antihypertensive treatment, on the structure and function of the basilar artery in rats.
  
  
  METHODS
  Rats were treated for 6 weeks with N omega-nitro-L-arginine methyl ester (50 mg/kg per day) alone or in combination with verapamil (100 mg/kg per day) or with trandolapril (1 mg/kg per day). Untreated rats served as controls. The structure and reactivity of perfused and pressurized basilar arteries were analyzed in vitro using a video dimension analyzer.
  
  
  RESULTS
  Systolic arterial pressure increased only in the nitro-arginine-treated group, as did the media-to-lumen ratio of the basilar artery. This structural alteration, which was prevented by verapamil and trandolapril, was mainly due to remodeling and not to growth. Chronic inhibition of the L-arginine pathway increased the response of the basilar artery to serotonin, while the opposite was found for endothelin. Verapamil and trandolapril prevented these functional alterations that seemed related to the changes in the vascular structure.
  
  
  CONCLUSIONS
  The remodeling and functional alterations of the basilar artery seem to depend mainly on the elevation of arterial pressure with little contribution of the L-arginine pathway. Furthermore, nitric oxide does not seem to be implicated in the modulation of normal cerebral vascular growth in vivo. However, hypertension-induced changes in vascular reactivity and structure could alter cerebral blood flow and eventually contribute to the development of stroke in this model of hypertension.
authors.affiliation: Department of Cardiology, University Hospital, Bern, Switzerland.
authors.forename: P
authors.initials: P
authors.lastname: Moreau
authors.forename: H
authors.initials: H
authors.lastname: Takase
authors.forename: C F
authors.initials: CF
authors.lastname: Küng
authors.forename: M M
authors.initials: MM
authors.lastname: van Rooijen
authors.forename: T
authors.initials: T
authors.lastname: Schaffner
authors.forename: T F
authors.initials: TF
authors.lastname: Lüscher
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001120:Arginine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology; D001488:Basilar Artery / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004195:Disease Models, Animal; D016232:Endothelins / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D007211:Indoles / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D051381:Rats; D011921:Rats, Inbred WKY; D012701:Serotonin / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology; D014741:Video Recording
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D016232:Endothelins; D004791:Enzyme Inhibitors; D007211:Indoles; D014665:Vasodilator Agents; C052035:trandolapril; D009569:Nitric Oxide; D012701:Serotonin; D001120:Arginine; D014700:Verapamil; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester