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

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Diphenhydramine and meclastine, two antagonists of histamine (H) H1 receptors completely suppressed the GH-releasing effect of eserine, while cimetidine, an H2 receptor antagonist, only blunted and delayed it. Two long-lasting serotonin (5-HT) receptor antagonists, metergoline and pizotifen, partially or completely suppressed, respectively, GH release evoked by eserine, whereas fenfluramine, a releaser of neuronal stores of 5-HT and hence a functional activator of 5-HT neurotransmission, was ineffective in this context. Pimozide, a long-acting dopamine receptor antagonist, abolished the effect of eserine, whereas domperidone, which has the same pharmacological properties but does not cross the blood brain barrier, failed to do so. Finally, phentolamine, an antagonist of alpha-adrenoceptors, and propranolol, a beta-adrenergic antagonist, were completely ineffective in preventing the rise in plasma cGH levels induced by eserine, as was naloxone, an antagonist of opiate receptors. All these data demonstrate that, although cholinergic mechanisms are involved in the mechanism(s) underlying cGH release, the final common pathway for GH secretion is not cholinergic. Preservation of dopaminergic and H1 neurotransmission, probably within the blood barrier, is needed to allow the neuroendocrine transduction of cholinergic inputs, whereas the role of 5-HT neurotransmission remains uncertain.
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PMID:Activation of the cholinergic system and growth hormone release in the dog: functional interactions with other neurotransmitters. 298 38

To throw light onto the mechanism(s) by which the cholinergic system influences growth hormone (GH) release, the effects of two muscarinic receptor blockers, pirenzepine and atropine, and of an acetylcholinesterase inhibitor, pyridostigmine bromide, on the GH response to GHRH-44 were studied in 19 normal volunteers. Moreover, the effects of pirenzepine administration on plasma GH levels both in basal conditions and after stimulation by GHRH-44 and TRH were studied in 9 acromegalics. Both pirenzepine (0.6 mg/kg i.v., 5 min before GHRH) and atropine (1 mg i.m., 15 min before GHRH) blunted the GH response to GHRH (1 microgram/kg i.v. bolus) (area under the response curve, AUC: 81.3 +/- 17.3 vs. 481.2 +/- 211.3 ng/ml/h for pirenzepine and 100.2 +/- 27.0 vs. 364.7 +/- 81.0 ng/ml/h for atropine; p less than 0.01). Pyridostigmine (120 mg orally, 30 min before GHRH) induced a variable but significant (p less than 0.02) rise in basal plasma GH levels and, furthermore, an unequivocal potentiation of the GH response to GHRH (AUC: 1044.6 +/- 245.3 vs. 481.2 +/- 211.3 ng/ml/h; p less than 0.01). In all but one acromegalics 0.6 mg/kg i.v. pirenzepine was unable to modify the basal GH levels whilst it showed a variable inhibitory effect on the GH response to GHRH. The GH response to TRH (200 micrograms i.v. bolus) was instead unmodified by pirenzepine. In conclusion, muscarinic receptor blockade inhibits while cholinergic potentiation seems to positively modulate the GH response to GHRH. Therefore, the cholinergic system seems to positively modulate the GHRH effect on somatotrophs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic involvement in the growth hormone releasing hormone-induced growth hormone release: studies in normal and acromegalic subjects. 309 9

Cholinesterase inhibitors induce changes in plasma hormones in the rat. Since these compounds induce hypothermia the question has been raised as to whether the endocrine responses are secondary to the fall in core temperature. The time course of the changes in temperature and plasma levels of corticosterone, growth hormone and prolactin have been examined following injection of diisopropylphosphofluoridate (DFP), soman or physostigmine. All three cholinesterase inhibitors caused an initial rise in corticosterone; DFP decreased growth hormone; physostigmine reduced prolactin. The time course of the hypothermia after DFP and soman did not correlate with that of the rise in corticosterone. The data do not suggest that the hormone changes are secondary to the temperature change.
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PMID:Relationship between the temperature and endocrine changes induced by cholinesterase inhibitors. 358 58

To investigate the ontogenesis of potential cholinergic influences on growth hormone secretion we administered the cholinesterase inhibitor neostigimine, (120 micrograms/kg) to fetal sheep (n = 16) between 77 and 143 days of gestation and to infant lambs (n = 5). Neostigmine administration was associated with a marked rise in fetal growth hormone concentrations. The integrated release of growth hormone in the hour following fetal neostigmine administration was 2880 +/- 425 ng.min/ml compared to -618 +/- 206 ng . min/ml (P less than 0.001) following saline administration (n = 19). There was no relationship between gestational age and the response to neostigmine. In the infant lamb, neostigmine was associated with a lesser (P less than 0.001) but significant (P less than 0.02) growth hormone response. The integrated release was 704 +/- 410 ng . min/ml (n = 5) compared to -44 +/- 40 ng . min/ml following saline (n = 11). The fetal response to neostigmine was abolished by the administration of atropine (200 micrograms/kg bolus followed by 400 micrograms/kg per h infusion) 5 min prior to neostigmine (n = 4). This demonstrates that the effect of neostigmine was mediated by muscarinic receptors. Atropine itself had no effect on fetal growth hormone release (n = 6). In vitro binding studies with the muscarinic ligand, 1-quinuclidinyl [phenyl-4 (n) -3H] benzilate) were performed on homogenates of fetal (n = 3) and adult (n = 3) pituitaries. Scatchard analysis demonstrated both a high affinity and low affinity binding site. The concentration per mg. of original tissue of each of these binding sites was higher (P less than 0.05) in fetal than adult homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscarinic influences on growth hormone secretion in the fetal and neonatal sheep: pharmacological studies and in vitro binding studies. 407 57

Cholinesterase activity of brain and content of growth hormone and prolactin in the pituitary were compared after short-term (3 days) and long-term (14 days) treatment with paraoxon in male and female rats. Within 3 days cholinesterase activity was reduced to between 5 and 15 percent of that in controls. The content of growth hormone in the pituitary was increased in long-term experiments by 50 percent. This increase in paraoxon-treated animals-suggests a possible role of a cholinergic mechanism in the regulation of growth hormone secretion.
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PMID:Paraoxon: effects on rat brain cholinesterase and on growth hormone and prolactin of pituitary. 506 Dec 47

In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) or the cholinergic muscarinic receptor agonist oxotremorine (0.25 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Complete suppression of the GH-releasing effect of eserine and oxotremorine was induced by blockade of cholinergic muscarinic receptors by atropine (80 or 20 micrograms/kg, 30 min before) but not by scopolamine-N-butyl bromide (0.8 mg/dog, 30 min before), an anticholinergic drug which does not cross the blood brain barrier (BBB). In contrast, activation of cholinergic nicotinic receptors by nicotine (6 mg) failed to alter resting cGH concentrations, and pre-treatment with the nicotinic receptor blocker mecamylamine (5 mg, 30 min before) did not counteract the GH-releasing effect of eserine. Other cholinomimetic drugs, e.g. pilocarpine, 4-aminopyridine, carbachol and bethanechol failed to induce a rise in plasma cGH concentrations. These data indicate that: 1) cholinergic muscarinic but not nicotinic receptors located in the central nervous system (CNS) inside the BBB play a facilitatory role in tonic cGH release; 2) pharmacologically distinct muscarinic receptors may exist in the CNS.
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PMID:Effect of agonists and antagonists of cholinergic neurotransmission on growth hormone release in the dog. 630 74

We examined the possibility that abnormalities of growth hormone (GH) release in cirrhotic patients were related to a reduction in the ratio of branched chain amino acids (BCAAs) to aromatic amino acids (AAAs) in plasma. The intravenous infusion of 250 micrograms of thyrotropin-releasing hormone (TRH) caused a significant rise in plasma GH greater than 5 ng/ml and more than twice as much as the basal levels in 7 out of 15 patients (responders) but an insignificant rise in the remaining patients (non-responders). The difference in the basal GH level was not significant. The oral glucose load suppressed plasma GH in all of the normal subjects and 6 of 7 non-responders, while it was elevated in 6 of 7 responders and one of the non-responders. The ratio of BCAAs to AAAs in the plasma of cirrhotic patients was 1.21 +/- 0.38, which was significantly lower than that of normal subjects (3.31 +/- 0.42, p less than 0.01). In addition, there was a significant difference between responders and non-responders in the ratios (0.96 +/- 0.22 vs 1.42 +/- 0.36, p less than 0.05). An inversely significant correlation (p less than 0.05) between the ratios of BCAAs to AAAs in plasma and the peak levels of GH after TRH injection was observed when all subjects were combined, but no correlation was found between the ratios and the peak levels of GH after oral glucose loading. There were also significant correlations (p less than 0.01) between the ratios and various parameters including the serum albumin, cholinesterase and indocyanine green disappearance rate constant (KICG).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interrelation between plasma amino acid composition and growth hormone secretion in patients with liver cirrhosis. 644 Jul 84

In 20 patients who underwent open-heart surgery, the plasma concentrations of glucose, insulin, glucagon, growth hormone, free hemoglobin, and cholinesterase were measured before, during and after pulsatile and continuous perfusion. Pulsatile flow was achieved by modification of a roller pump to effect rapid acceleration and slowing. The driving motor was interfaced with a control module to enable ECG-triggered perfusion. In addition to the clinical studies, investigations were performed in 9 dogs to assess the effects of pulsatile and continuous perfusion on liver and pancreas flow during total bypass. During pulsatile perfusion there was a significant increase in insulin which, however, was clearly diminished in relation to glucose levels. The response of the beta-cells was markedly more compromised after continuous than pulsatile perfusion. The secondary postoperative increase in insulin can be accounted for by intravenous administration of glucose and, particularly, after pulsatile perfusion, indicates an almost completely normal response of pancreatic beta-cells. As opposed to the effects of continuous perfusion, the low glucose, glucagon, and growth hormone levels, the insulin increase during and after pulsatile perfusion as well as normal cholinesterase values observed in association with pulsatile perfusion appear to be the result of improved pancreatic and hepatic function. This contention is supported by the experimental finding of significantly increased pancreas and liver perfusion during pulsatile perfusion.
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PMID:[Clinical and experimental studies on pulsatile and continuous flow during extracorporeal circulation (author's transl)]. 700 92

Endogenous cholinergic stimulation, produced by the intravenous injection of edrophonium (10 mg), an acetylcholinesterase inhibitor, into 8 normal human subjects, resulted in an increase in the mean (+/- SE) serum growth hormone (GH) concentration from 0.6 +/- 0.1 ng/ml to 5.6 +/- 1.4 ng/ml (p < 0.01) at 40 min with no changes in serum prolactin. In 2 subjects sampled for 140 min. maximum serum GH levels of 19.4 and 10.2 ng/ml (from baseline values of 0.4 and 0.6 ng/ml) occurred at 65 min after edrophonium injection. Thus, enhancement of endogenous cholinergic activity stimulates GH secretion, providing further evidence for a role of cholinergic mechanisms in the physiologic regulation of GH secretion in man. The theoretical possibility that excessive endogenous cholinergic activity might be involved in the pathophysiologic regulation of GH secretion in man. The theoretical possibility that excessive endogenous cholinergic activity might be involved in the pathophysiologic regulation of GH secretion in acromegaly was not, however, supported, since methscopolamine (0.5 mg s.c.), a cholinergic antagonist, did not reduce mean serum GH levels in 3 acromegalic patients.
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PMID:Endogenous cholinergic modulation of growth-hormone secretion in normal and acromegalic humans. 740 75

Pyridostigmine (PST), a cholinesterase inhibitor, induces a clear growth hormone (GH) release in man by suppression of hypothalamic somatostatin (SRIH). Somatostatin suppresses thyrotrophin (TSH) release in rats and men. Earlier studies showed that the thryotrophin-releasing hormone (TRH)-induced TSH response was not altered by 60-120 mg of PST. We studied whether a larger dose (180 mg) of PST can increase the TSH response to TRH. Six healthy young men were studied with the following six tests: (Test 1) 200 micrograms of TRH i.v.; (Test 2) 180 mg of PST po; (Test 3) three different doses of PST (60, 120, 180 mg) + TRH; (Test 4) 100 micrograms of octreotide (SMS) i.v.; (Test 5) SMS + TRH; (Test 6) PST + SMS + TRH. A large dose of PST (180 mg) significantly augmented GH, TSH and prolactin responses to TRH, while smaller doses of PST (60 and 120 mg) did not significantly increase the responses of GH and TSH. While the increased TRH-induced prolactin response by PST was not suppressed by SMS, the increased responses of GH and TSH were suppressed remarkably by SMS. Most of the subjects noticed a mild to moderate abdominal pain, nausea and muscular fasciculation after the administration of a large dose of PST administration. These data suggest that suppression of hypothalamic SRIH secretion by 180 mg of PST can augment the TSH response to TRH. However, the considerable side effects should be minimized before clinical application of the combined PST-TRH test.
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PMID:Combined pyridostigmine-thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men. 758 70


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