Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.1.7 (
acetylcholinesterase
)
28,390
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. The interaction of hexafluorenium with acetylcholine, carbachol and suxamethonium with regard to the depolarization of the end-plate of rat diaphragm was studied. The depolarization was measured with the moving meniscus technique of Fatt. The competitive antagonist d-tubocurarine was included in the studies. 2.
Hexafluorenium
inhibited
acetylcholinesterase
in the end-plate. 3. The receptors in the end-plate were desensitized by carbachol and suxamethonium.
Hexafluorenium
enhanced the desensitization by suxamethonium. d-Tubocurarine had no direct influence on desensitization 4. The desensitization of the receptors in rat diaphragm is compatible with a cyclic model of desensitization. 5. The desensitizing interaction of hexafluorenium with the receptors may explain the non-competitive antagonism with depolarizing drugs with regard to the depolarization of the end-plate and the synergism with these drugs with regard to the paralysis of the indirectly stimulated muscle reported earlier. 6. The affinities of carbachol, suxamethonium and d-tubocurarine to the sensitive receptors are 4.9, 5.2 and 6.8, respectively.
...
PMID:The desensitizing interaction of hexafluorenium with the cholinergic receptor in the diaphragm of the rat. 84 69