title: Internal mammary artery grafts reactivity in hypertensive patients: role of stretching in extraendothelial nitric oxide.
abstract: BACKGROUND
  The internal mammary artery (IMA) used in bypass coronary surgery remains efficient for a longer time than other grafts, such as saphenous veins; however, its biological characteristics are incompletely defined.
  
  
  OBJECTIVE
  To compare in IMA grafts from hypertensive (HT) and normotensive (NT) patients the presence of endothelium and their functionability, the response to passive stretching and basal tone, the reactivity to exogenous vasoconstrictors, the role of stretching in NO release, and the possible extraendothelial NO source.
  
  
  RESULTS
  IMA rings contractility, presence of endothelium, and nitrite release were studied. An endothelial dysfunction associated with hypertension was found. IMA rings from HT had an impaired response to passive stretching, resulting in a decreased relaxation. All IMA grafts had an increased basal tone demonstrated by relaxation to SNP; however, a lesser response was found in HT. Interestingly, it was demonstrated that NO release was present in IMA grafts, despite an endothelial dysfunction and that stretching increased NO release. This effect was inhibited by Ca2+ -free media, L-NAME and a specific neuronal NO synthase (nNOS) inhibitor. Furthermore, the demonstration of the presence of nNOS in smooth muscle cells by immunohistochemistry supports a role of extraendothelial NO.
  
  
  CONCLUSIONS
  We demonstrate the impact of hypertension in IMA grafts producing increased endothelial dysfunction, reduced response to passive stretching, increased basal tone, and impaired responsiveness to exogenous vasoconstrictors and NO release. A specific role of stretching in extraendothelial NO release was demonstrated, which may have an important role in the outcome of IMA grafts due to the protective actions of NO, even in the absence of the endothelium.
authors.affiliation: Dpto. Biomédico (Or. Fisiología), Facultad de Medicina, Universidad Nacional de Tucumán, INSIBIO-CONICET, Tucumán, Argentina.
authors.forename: Claudio M Joo
authors.initials: CM
authors.lastname: Turoni
authors.forename: María Peral
authors.initials: MP
authors.lastname: de Bruno
authors.forename: Alfredo
authors.initials: A
authors.lastname: Coviello
authors.forename: Rodrigo O
authors.initials: RO
authors.lastname: Marañón
authors.forename: Ramón N
authors.initials: RN
authors.lastname: Herrera
authors.forename: Juan
authors.initials: J
authors.lastname: Muntaner
authors.forename: Víctor
authors.initials: V
authors.lastname: Proto
mesh_terms: D000368:Aged; D000804:Angiotensin II / Q000494:pharmacology; D001696:Biomechanical Phenomena; D004730:Endothelium, Vascular / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008323:Mammary Arteries / Q000187:drug effects / Q000503:physiopathology*; D008875:Middle Aged; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D013314:Stress, Mechanical; D014664:Vasodilation / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D000804:Angiotensin II; D009599:Nitroprusside; D009569:Nitric Oxide; D011189:Potassium Chloride; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine