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

The studies were performed on operation material from 17- to 63-year-old patients and on fetuses at 19-23 weeks gestational age. Formaldehyde histofluorescence showed the presence of numerous perivascular adrenergic nerves around pial and intracerebral vessels, the carotid system being better supplied than the vertebral system. Cholinergic nerves, visualized by the cholinesterase technique, followed the adrenergic fibers in the plexus formations of the pial arterial system. Histamine-containing mast cells, often with a perivascular distribution, were located with the o-phthaldiadehyde method. Transmural electrical stimulation of the perivascular nerves contracted isolated pieces of pial arteries in a frequency-dependent manner, and the response was inhibited by the adrenergic nerve blocking agent, guanethidine. On the basis of the relative potency of various amines and related compounds in producing a motor response of isolated pial arteries, and the mode of inhibition caused by specific antagonists, various amine receptors could be demonstrated: adrenergic alpha-receptors (mediating contraction) and beta-receptors (dilation), cholinergic muscarinic receptors (dilation) and histamine H2-receptors (mediating dilation). Thus, the amine mechanisms demonstrated in human brain vessels appear to be principally the same of those shown in more extensive studies on laboratory animals.
 ...
PMID:Autonomic nerves, mast cells, and amine receptors in human brain vessels. A histochemical and pharmacological study. 18 80

The effects of histamine, applied by microiontophoresis onto spontaneously-active medullary neurones were investigated in the rat. Histamine caused current-dependent excitation of these neurones, an action that is at variance with previous studies in the cat. The nature of the receptor mediating these effects was examined using a number of agonists with differing potencies at peripheral H1- and H2-receptors. The precursor of histamine, L-histidine and the metabolite, N-telemethylhistamine did not mimic the effects of histamine while the H2-agonist, 4-methylhistamine caused similar but weaker excitation. The extent of excitations produced by the H1-agonists, 2-pyridylethylamine, 2-methylhistamine and 2-thiazolylethylamine could be related to their activity at H2-receptors. Metiamide was ineffective in antagonising responses to histamine and related agonists as was mepyramine. The H2-antagonist ranitidine, however, proved a good antagonist of responses to histamine and the H1- and H2-agonists, despite an unrelated excitatory action which may be linked to inhibition of cholinesterase. It is concluded that the excitatory effects of microiontophoretically-applied histamine and the agonists on medullary neurones in the rat is probably a result of activation of H2-receptors.
 ...
PMID:Histamine-induced excitation of spontaneously active medullary neurones in the rat brain is mediated by H2-receptors. A microiontophoretic study using H1- and H2-agonists and antagonists. 286 36

Histamine release from the basophil leucocytes of patients with apparently non-immune, anaphylactiod reactions to neuromuscular blockers ( NMB ) has been studied in vitro. Substantial release was obtained in the majority of patients with clinical reactions, with little or no release in normal subjects. The chemical specificity and selectivity varied in individual patients: each individual reacting to one agent or a particular combination of NMB drugs. The test was of considerable diagnostic and predictive value. We studied some of the characteristics of the histamine release process and the effect of certain modulators. The findings strongly suggest a non-cytotoxic secretory process requiring the presence of two quaternary ammonium groups as suggested by the rarity of release with tubocurarine; inhibition of succinyldicholine (suxamethonium)-induced histamine release by serum cholinesterase treatment, acetylcholine and tubocurarine; and the bell-shaped dose-response curve, particularly with suxamethonium. Histamine release by all NMB was completely inhibited in calcium-free medium, and markedly potentiated by deuterium oxide, a microtubule stabilizer. Both tachyphylaxis (by prior exposure to the specific agent in absence of calcium), and cross-tachyphylaxis with anti-IgE were elicited.
 ...
PMID:Characteristics of basophil histamine release by neuromuscular blocking drugs in patients with anaphylactoid reactions. 620 65

In this study, the effects of mepyramine (H1-receptor antagonist), famotidine (H2-receptor antagonist), physostigmine (a cholinesterase inhibitor) and atropine (muscarinic-receptor antagonist) have investigated on the formalin-induced nociception in rats. The effects of mepyramine and famotidine have also examined on nociceptive changes induced by physostigmine and atropine. Nociception was induced by intraplantar injection of formalin (50 microL, 1%) into the right hind paw and the time spent licking and biting of the injected paw, was taken as a measure of pain. Formalin induced a marked biphasic (first phase: 0-5 min and second phase: 15-45 min) pain response. The used drugs did not change the first phase of formalin-induced pain. Subcutaneous injection of physostigmine significantly (p<0.05) suppressed pain. Subcutaneous injection of atropine alone did not change the intensity of pain, but pretreatment with atropine significantly (p<0.05) prevented physostigmine-induced antinociception. Intraperitoneal injections of mepyramine and famotidine significantly (p<0.05) decreased pain response. Mepyramine did not significantly change, but famotidine significantly (p<0.05) prevented analgesic effect of physostigmine on pain. Atropine did not inhibit the antinociceptive effects of both mepyramine and famotidine on formalin-induced nociception. These results indicate that physostigmine through muscarinic cholinergic receptors suppresses the pain induced by formalin. Both H1 and H2 receptor antagonists produce antinociception. Histamine H2, but no H1 antagonists may be involved in physostigmine-induced antinociception.
 ...
PMID:Effects of mepyramine and famotidine on the physostigmine-induced antinociception in the formalin test in rats. 1926 Mar 35