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Possible Interaction: Folic Acid Antagonists and Tubocurarine

Research Papers that Mention the Interaction

Antagonists of nAChRs blocked NIC-induced responses with a rank order of potency of d-tubocurarine (d-Tubo)=mecamylamine (MEC)>dihydro-beta-erythroidine (DHbetaE) in A3B2 cells and MEC=DHbetaE>d-Tubo in A4B2.2 cells.
Neuropharmacology  •  2000  |  View Paper
Inhibition of acetylcholinesterase by antagonists resulted in an increased dose of tubocurarine but an unchanged resistance ratio between the diaphragm and the EDL.
Anesthesiology  •  2005  |  View Paper
It is concluded that this depressive action on transmitter output contributes to onset of tetanic fade and that when higher concentrations of these antagonists are used this inhibitory action of TC and HEX may override autoreceptor feedback regulation.
Neuroscience Letters  •  1995  |  View Paper
The antagonist d-tubocurarine blocked the activation of the channels, whereas hexamethonium had only a weak effect; similar properties have been described for nicotinic insect receptors in situ.
The Journal of general physiology  •  1987  |  View Paper
Both d-tubocurarine and Cch had concurrent antagonistic interrelations in respect to their action on the quantum content of EPP.
Biulleten' eksperimental'noi biologii i meditsiny  •  1979  |  View Paper
The block produced by tubocurarine , hexamethonium and decamethonium increases with the agonist concentration, an observation which supports a 'sequential' scheme in which the antagonist blocks the 'open' channel-receptor complex.
The slow relaxations observed with tubocurarine and hexamethonium are speeded by an increase of the antagonist concentration; the slow relaxations observed with decamethonium are slowed by an increase of the decamethonium concentration.
The Journal of physiology  •  1979  |  View Paper