Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Using a K+-sensitive extracellular electrode, we attempted to determine whether cholinergic stimulation of the simian palm eccrine sweat gland is associated with transient net K+ efflux as in other exocrine glands. 2. When isolated secretory coils placed in a glass capillary were continuously superfused (method A), 32% of total cellular K+ was lost during 3 min of stimulation with methacholine (MCh) followed by K+ reuptake when stimulation was stopped. 3. When secretory coils were stimulated in a small chamber (without continuous superfusion, method C), MCh (5 x 10(-6) M)-induced maximal K+ efflux as determined by the peak level of extracellular K+ concentrations was dose dependent, inhibited by atropine but not altered by a cholinesterase inhibitor, physostigmine (1.3 x 10(-5) M). Thus the peak K+ level was used as a measure of K+ efflux throughout the study. 4. Phenylephrine (10(-4) M) and A23187 (5 x 10(-6) M) also induced K+ efflux but to a lesser extent than did MCh. 5. Ouabain (10(-3) M)-induced K+ loss was 2.4-fold higher than the peak level of MCh-induced K+ efflux. 6. In a Ca2+-free medium with added EGTA, inhibition of K+ efflux was only partial in the first MCh stimulation but progressively increased on repeated stimulation, suggesting that cytoplasmic or membrane Ca2+ not readily accessible to EGTA may be important for K+ efflux. Inhibition of K+ efflux in the Ca2+-free medium was completely reversed on subsequent addition of Ca2+. 7. Five millimolar Ba2+ partially inhibited MCh-induced K+ efflux. 8. 10(-4) M-bumetanide itself caused a small K+ loss and strongly inhibited the subsequent MCh-induced K+ loss. 9. MCh-induced K+ loss was drastically inhibited in the low-Cl- (by replacing with gluconate- or methylsulphate-) or low-Na+ (by replacing with Tris+) medium. 10. K+ efflux occurs predominantly across the basolateral membrane. 11. Vinblastine at 10(-4) M, which completely inhibits sweat secretion (our unpublished results), however, showed no effect on MCh-induced K+ efflux. 12. We conclude that the transient net K+ efflux associated with MCh stimulation constitutes a crucial primary ionic event in cholinergic eccrine sweat secretion as in other exocrine secretory cells.
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PMID:K+ efflux from the monkey eccrine secretory coil during the transient of stimulation with agonists. 315 70

1. The acetylcholine content of cortical slices from rat brain, was determined after incubation for 30 min in a medium containing acetylcholine (4 mug/ml.). The cholinesterase activity of the slices had been inhibited by pretreatment with 3,3-dimethyl-n-butyl 2-methylphosphonofluoridate (soman).2. Acetylcholine accumulated in the tissue slices, up to a concentration of about six times that in the medium.3. The uptake of acetylcholine was partly inhibited by potassium in high concentrations.4. Hemicholinium-3, O-ethyl S-diethylaminoethyl ethylphosphonothiolate, physostigmine, atropine and choline, in that order of potency, inhibited the accumulation of acetylcholine in the cortical slices, but soman and ethyl N,N-dimethyl phosphonoamidocyanate (tabun) had no effect on the uptake of acetylcholine.5. Substances interfering with energy metabolism, such as 2,4-dinitrophenol, oligomycin, sodium azide, amylobarbitone sodium and p-chloromercuribenzoate inhibited the uptake of acetylcholine. Ouabain had little inhibitory effect.6. In anaerobic conditions the accumulation of acetylcholine in the tissue slices was nearly blocked.7. The uptake of acetylcholine in the tissue slices was dependent on temperature. The Q(10) was about 2.8. Autoradiography of sections from slices in which (3)H-acetylcholine had accumulated showed a diffuse distribution of radioactivity in the cytoplasm of all cells. There was no visible preference for certain cells or cell structures.
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PMID:The influence of drugs on the uptake of acetylcholine by slices of rat cerebral cortex. 576 84

The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40% of those causing arrhythmias. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemo-inhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anti-cholinesterase, affected the response of the carotid chemoreceptors to ouabain. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+--K+-ATPase-inhibiting property of ouabain.
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PMID:Effects of ouabain on carotid body chemoreceptor activity in the cat. 687 75