Tetrodotoxin-resistant relaxation to transmural nerve stimulation in canine saphenous veins: a possible neural origin

Abstract

Transmural nerve stimulation following sympathetic (guanethidine 10−4 mol/L, phenoxybenzamine 2 × 10−5 mol/L, propranolol 2 × 10−6 mol/L) and muscarinic blockade (atropine 5 × 10−5 mol/L) produces a relaxatory response in canine saphenous veins contracted with prostaglandin F2α. This relaxatory response was shown previously to be resistant to tetrodotoxin. Transmural nerve stimulation (10 V, 1.0 ms) was applied as intermittent trains of stimuli of 30 s duration at frequencies of 1–32 Hz. The veins showed a frequency dependent relaxation (maximum 2.65 ± 0.20 g). The stimulations were repeated in the presence of lignocaine (10−3 mol/L), apamin (10−8 mol/L), ascorbic acid (10−4 mol/L), or catalase (50 μg/mL). The relaxatory response was unaffected by apamin, scorpion toxin, superoxide dismutase, ascorbic acid, and catalase (p > 0.05). However, lignocaine (10−3 mol/L) reduced significantly the relaxatory response to transmural nerve stimulation in this preparation (p < 0.05). In a separate group of veins, lignocaine (10−3 mol/L)l abolished the contractile response to transmural nerve stimulation with little effect upon the contractile response to exogenous noradrenaline and the relaxatory responses to isoprenaline and sodium nitrite. These findings support the proposition that the nonadrenergic, noncholinergic tetrodotoxin-resistant relaxatory response observed with transmural nerve stimulation in the canine saphenous vein is mediated by a neural mechanism.