ATTENUATED INHIBITION OF ADRENERGIC CONTRACTION BY NITRIC-OXIDE IN INJURED GUINEA-PIG FEMORAL-ARTERY

The present study aimed to examine the altered modulation of adrenergi c contraction by nitric oxide and sensory neuropeptides in balloon-inj ured muscular artery. A guinea pig femoral artery (GPFA) was injured b y 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 wee ks after injury (CO, IO, C2, I2, C8, and I8). Isometric tension was me asured 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, exc ept for IO, N-G-nitro-L-arginine methyl ester (L-NAME, 10(-6) M) induc ed significant augmentation of perivascular nerve stimulation (PNS)evo ked adrenergic contraction, which was blocked by L-arginine (3 x 10(-4 ) M). The degree of L-NAME augmentation in I8 was significantly smalle r than that in C8 and I2. Capsaicin (10(-6) M) did not significantly a ffect PNS-contraction in any group, indicating that there was no senso ry neuropeptide involvement in this contraction. In I8, acetylcholine (10(-6) M)-induced relaxation after noradrenaline (10(-5) M)-precontra ction was significantly smaller than that seen in the other groups, ex cept for IO, which was lacking in acetylcholine-induced relaxation. Hi stologically, injured GPFAs showed progressive intimal thickening. The present findings thus showed attenuated nitric oxide-mediated inhibit ion of adrenergic contraction, accompanying intimal thickening, in bal loon-injured muscular artery, 8 weeks after injury.