Effect of quinidine and tetrodotoxin on the activation of non-adrenergic nerves in guinea-pig trachealis muscle.
Activation of non-adrenergic neurones in guinea-pig trachealis muscle was accomplished by electrical field stimulation and by the neurotoxin aconitine, in the presence of atropine and propranolol. Aconitine (10(-5) M) activated non-adrenergic neurones more slowly, but was as efficacious as supramaximal field stimulation (70 V, 1 msec, 1-100 Hz), producing 70-80% of the maximal relaxation to forskolin or theophylline. Quinidine (3 X 10(-5) M-3 X 10(-4) M) and tetrodotoxin (5 X 10(-9) M-3 X 10(-6) M) blocked relaxations to aconitine and field stimulation, without affecting smooth muscle relaxant responses to forskolin. The results suggest that the non-adrenergic inhibitory effects of quinidine are related to its presynaptic local anaesthetic actions, rather than to postsynaptic receptor blockade of the non-adrenergic inhibitory neurotransmitter.
D000157:Aconitine / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects*; D005576:Colforsin / Q000494:pharmacology; D004558:Electric Stimulation; D006168:Guinea Pigs; D066298:In Vitro Techniques; D009130:Muscle, Smooth / Q000502:physiology*; D009474:Neurons / Q000187:drug effects*; D011802:Quinidine / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology*; D014132:Trachea / Q000294:innervation*
D005576:Colforsin; D013779:Tetrodotoxin; D011802:Quinidine; D000157:Aconitine