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)

The spontaneously hypertensive rat (SHR)--animal model for human essential hypertension--develops a generalized arteriopathy. The present paper discusses the atherogenic influence of hypertensive arterial lesions. The following changes in the intima might influence its permeability and barrier function, increase the trapping effect and stimulate the smooth muscle cell proliferation: the hyper-reactivity of endothelial cells; the decreased thickness of endothelial cell periphery; the reduced intercellular junction pathways; the increase in basal lamina and glycosaminoglycan sub-endothelial material; the mononuclear cell infiltrations; the widened fenestrae in the internal elastic lamina. Some hypertensive changes of the tunica media may also interact with atherogenic process through reduced smooth muscle cell lipolytic capabilities, slowed transmural diffusion, perturbed efflux, aggravated media hypoxia, namely: the decrease in esterase and cholinesterase activities, the activations of some lysosomal enzymes, the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness and transmural passage; the modified smooth muscle cell behavior.
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PMID:[Hypertensive arteriopathy and atherogenesis: cellular and molecular interactions]. 310 95

Polymorphism of serum cholinesterase (SCE, acylcholinacylhydrolase, EC 3.1.1.8) for the E1 locus was studied in the groups of the patients affected with schizophrenia, peptic ulcer, hereditary erythrocytopathies, tuberculosis, thyreotoxicosis, essential hypertension and rheumatic disease. Increased frequencies of I phenotypes (E1uE1a genotype) were found among patients with peptic ulcer (12.3%), hereditary erythrocytopathies (23.2%), and UF phenotypes (E1uE1f genotype) were observed among patients with schizophrenia (2.8%) and tuberculosis (5.4%). The increased frequencies of E1a and E1f alleles in these groups of patients were, as compared to the control group, statistically significant. The value of relative risk for peptic ulcer was 3.39 in individuals of the E1uE1a genotype, those being 3.62 for schizophrenia and 6.92 for tuberculosis in individuals of the E1uE1f genotype. The nature of the other associations is discussed.
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PMID:[Association of mutant alleles of serum cholinesterase with various multi-factorial and infectious diseases]. 347 79

Red cell Na-Li countertransport was measured in 78 normal subjects, 64 patients with essential hypertension, and 67 patients with hyperlipidemias. Both hypertensive and hyperlipidemic patients had elevated Na-Li countertransport compared to normal controls (p less than 0.001). Subjects with hyperlipidemia and hypertension had higher countertransport (p less than 0.02) than patients with only hyperlipidemia. Normotensive hyperlipidemic subjects had higher countertransport than normotensive and normolipidemic controls (p less than 0.02). This suggest that hypertension and high plasma lipids can influence independently the Na-Li countertransport. In another group of 52 normotensive subjects, Na-Li countertransport was positively correlated with serum total and free (unesterified) cholesterol, phospholipids and triglycerides. No correlations were found with HDL-cholesterol or HDL-phospholipids. A very high positive correlation was found between Na-Li countertransport and plasma acetylcholinesterase (p less than 0.005). These findings suggest that plasma lipids, probably through membrane lipids, can affect the maximal rate of the Na-Li exchange in red cells. The relationship between plasma or membrane lipids and cation transport should be further studied in erythrocytes and other cells.
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PMID:Elevation of red cell sodium-lithium countertransport in hyperlipidemias. 396 81

There is accumulating evidence that acetylcholinesterase (AChE might be involved in the transport of sodium across biological membranes. Consequently, because in primary hypertension abnormalities in the transport of sodium by red blood cells have been documented. AChE activities were measured in hemoglobin-free red-blood-cell membranes of patients with essential hypertension. In the absence of any effectors, the Michaelis constant of AChE for acetylcholine (Km) was 1.57 . 10(-5) mol/l, both in normotensives and in hypertensives. Sodium inhibited AChE at low substrate concentrations, whereas the enzyme was activated by sodium at moderate and high substrate levels. With increasing sodium, the substrate optimum was displaced toward higher substrate concentration. On the other hand, an inhibition of AChE by excess substrate could be demonstrated. Erythrocyte AChE activity of male patients with essential hypertension was no different from that of the normotensive controls. Therefore, abnormalities in electrolyte transport mechanisms reported in essential hypertension might be independent of AChE activity.
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PMID:Studies on erythrocyte acetylcholinesterase in essential hypertension. 713 36

Red cell acetylcholinesterase activity (AChE) has been studied in 58 patients suffering from essential hypertension; diastolic blood pressure values were about 130 mm or higher in 45 patients (group A) and lower in 13 (group B). The very significant increase (p < 0.001) of AChE activity in group A has been forced by the severity of systemic lesions. Meanwhile, the AChE values have been slightly increased, but not statistically significant in the patients of group B. These results are supporting the hypothesis that the blood pressure control can be mediated or normalized, at least in part, by cholinergic mechanisms.
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PMID:Erythrocyte acetylcholinesterase in essential hypertension. 744 Dec 35

Monitoring the genomic expression of patients in clinical trials for Alzheimer's disease (AD) can assist trial design and treatment response analysis. Here, we report on the identification in AD patients of blood-based transcriptomic signatures associated with treatment response of EHT 0202, a new compound with potential disease-modifying and symptomatic properties, in a 3-month, placebo-controlled, Phase IIA study aimed at determining the clinical safety, tolerability, and exploratory efficacy of EHT 0202 (40 and 80 mg bid) as adjunctive therapy to one cholinesterase inhibitor in mild to moderate AD patients. Genome-wide transcriptomic profiling was performed on blood samples taken prior to treatment and at study completion in a subpopulation of 60 AD patients selected as either the 10 worst disease decliners or the 10 best improvers of each treatment group, using ADAS-Cog scores as measure of disease severity. In the patients responding to EHT 0202, a pre-treatment (baseline) transcriptomic signature showed activation of pathways related to AD, CNS disorders, diabetes, inflammation, and autoimmunity, while a post-treatment signature indicated reduced activation of these pathways with induced metabolic and transcription stimulation. This pilot study demonstrates the utility of blood transcriptomic signatures used as biomarkers for predicting patient response or monitoring efficacy, for an administered therapeutic drug in a complex disease such as AD. For EHT 0202 or other AD drugs, such biomarkers may help to improve strategies to better identify appropriate patient populations for treatment, understand the drug mechanism of efficacy, and/or clarify the inherent subjectivity in most clinical endpoints used in this disease.
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PMID:Blood transcriptomic biomarkers of Alzheimer's disease patients treated with EHT 0202. 2323 80