title: Attenuated inhibition of adrenergic contraction by nitric oxide in injured guinea pig femoral artery.
abstract: The present study aimed to examine the altered modulation of adrenergic contraction by nitric oxide and sensory neuropeptides in balloon-injured muscular artery. A guinea pig femoral artery (GPFA) was injured by a newly developed silastic microballoon catheter. The contralateral GPFA served as the control. The studied GPFAs consisted of six groups; control (C) and injured (I) GPFA, isolated at 0 days, and 2 and 8 weeks after injury (C0, I0, C2, I2, C8, and I8). Isometric tension was measured in the presence of indomethacin (10(-5) M), to exclude effects of cyclooxygenase-generated eicosanoids. Endothelial removal with the catheter was confirmed by histological examination. In each group, except for 10, NG-nitro-I-arginine methyl ester (L-NAME, 10(-6) M) induced significant augmentation of perivascular nerve stimulation (PNS)-evoked adrenergic contraction, which was blocked by L-arginine (3 x 10(-4) M). The degree of L-NAME augmentation in I8 was significantly smaller than that in C8 and I2. Capsaicin (10(-6) M) did not significantly affect PNS-contraction in any group, indicating that there was no sensory neuropeptide involvement in this contraction. In I8, acetylcholine (10(-6) M)-induced relaxation after noradrenaline (10(-5) M)-precontraction was significantly smaller than that seen in the other groups, except for I0, which was lacking in acetylcholine-induced relaxation. Histologically, injured GPFAs showed progressive intimal thickening. The present findings thus showed attenuated nitric oxide-mediated inhibition of adrenergic contraction, accompanying intimal thickening, in balloon-injured muscular artery, 8 weeks after injury.
authors.affiliation: Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Matsuda
authors.forename: A
authors.initials: A
authors.lastname: Kawaguchi
authors.forename: J
authors.initials: J
authors.lastname: Tamai
authors.forename: M
authors.initials: M
authors.lastname: Uematsu
authors.forename: S
authors.initials: S
authors.lastname: Nagata
authors.forename: K
authors.initials: K
authors.lastname: Miyatake
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D002404:Catheterization; D004195:Disease Models, Animal; D005263:Femoral Artery / Q000473:pathology*; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D009569:Nitric Oxide; D001120:Arginine; D000109:Acetylcholine; D002211:Capsaicin; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine