Modification by strychnine and D-tubocurarine of cardiac vagal inhibition in dogs.
Intravenous infusion of strychnine or D-tubocurarine chloride attenuated the cardiac depressant action and fall in blood pressure produced by electrical stimulation of the right vagus nerve in dogs anesthesized with pentobarbitone sodium. The effects of exogenous acetylcholine on the heart and blood pressure (B.P.) were not modified by strychnine or D-turbocurarine. Physostigmine sulphate potentiated the effects of injected acetylcholine without modifying the effects of strychnine and D-tubocurarine on vagal transmission. Dimethylphenylpiperazinium bromide also produced its characteristic effects on the heart and B.P. in the presence of strychnine and D-tubocurarine. The results indicate that strychnine and D-tubocurarine inhibition of vagal transmission is not a result of blockade of peripheral cholinergic receptors or cardiac vagal ganglia. This inhibition occurs presumably via a preganglionic presynaptic action.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006321:Heart / Q000187:drug effects*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D013331:Strychnine / Q000494:pharmacology*; D014403:Tubocurarine / Q000494:pharmacology*; D014630:Vagus Nerve / Q000502:physiology*
D004246:Dimethylphenylpiperazinium Iodide; D013331:Strychnine; D000109:Acetylcholine; D014403:Tubocurarine