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)

In unanesthetized freely moving rats, microinjection of a variety of cholinergic agonists into the posterior hypothalamic nucleus (PHN) consistently produced an elevation in mean arterial pressure (MAP). Experiments were undertaken to pharmacologically characterize this cholinergic mechanism. Microinjection of carbachol (0.1--100 nmol) into the PHN elicited reproducible and dose-related increase in MAP (17--47 mm Hg) and variable changes in heart rate. Similar responses, although longer in onset and duration, were produced by microinjection of the cholinesterase inhibitors, neostigmine, physostigmine and echothiophate. The pressor responses produced by neostigmine and physostigmine, but not by carbachol, were shown to be dependent upon intact stores of acetylcholine in the PHN. Blockade of postsynaptic muscarinic receptors by prior microinjection of atropine abolished the rise in MAP to subsequent injection of cholinergic agonists; however, similar pretreatment with the antinicotinic agent, mecamylamine, was without effect. The peripheral mechanism through which a rise in MAP was produced by cholinergic stimulation of PHN was the sympathetic nervous system since i.v. injection of an alpha-adrenergic blocking agent, phentolamine, attenuated the pressor response to intrahypothalamic injection of carbachol or neostigmine. Adrenal catecholamine release or vasopressin release were not important mechanisms in this regard. From this study we conclude that within the rat PHN there exists a muscarinic, cholinergic mechanism which, upon activation, mediates a rise in MAP through an increase in sympathetic tone.
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PMID:Pharmacological study of a cholinergic mechanism within the rat posterior hypothalamic nucleus which mediates a hypertensive response. 42 Nov 41

Gastric evacuation and small bowel propulsion were greatly retarded two hours after laparotomy in the rat. Adrenal demedullation, chemical sympathectomy with 6-hydroxydopamine or treatment with a cholinesterase inhibitor (Neostigmin), an alpha-receptor blocker (Dibenyline) or metoclopramide (Primperan) did not improve the gastric evacuation. Chemical sympathectomy or treatment with metoclopramide, however, significantly improved small bowel propulsion. A significant reflux of duodenal contents to the stomach was found in several animals treated with the cholinesterase inhibitor or subjected to adrenal demedullation.
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PMID:Effects of sympatho-adrenal activity and pharmacological treatment on gastrointestinal propulsion in the early postoperative period. An experimental study in the laparotomized rat. 106 28

In the present review an update on the medical therapy of open-angle glaucoma is given. Antiglaucomatous drugs that are rarely or no longer indicated are briefly discussed, as are the current medical therapy and perspectives of the medical management of glaucoma. In light of the pharmacological profiles of current antiglaucomatous agents, irreversible cholinesterase inhibitors, are out of date, and higher concentrations of clonidine eye drops and aqueous preparations of epinephrine-hydrocloride are also old-fashioned. The spectrum of current antiglaucomatous drugs is outlined and perspectives are indicated that will enrich our antiglaucomatous drug armamentarium in the near future. In this respect the development of pro-drugs and, new designs in the pharmaceutical preparation of traditional drugs are emphasized. In the field of new agents special emphasis is placed on topically applicable carbonic anhydrase inhibitors, the selective alpha-2-agonist apraclonidine and IOP-lowering prostaglandin derivatives. A series of agents is presented that are still experimental.
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PMID:[Drug therapy of glaucoma]. 208 99

Fenitrothion was administered orally to mice or rats in daily doses of up to 1/25 of the LD50 for 14 days, and numbers of splenic plaque-forming cells against sheep red blood cells (SRBC-PFC), one of the most common immune parameters, were measured. Splenic SRBC-PFC number was suppressed by fenitrothion only in rats which received 30 mg/kg body weight (bw) of the compound. Other immune parameters, including the arthus reaction, delayed-type hypersensitivity, and activities of macrophages and natural killer cells in rats, were not influenced by fenitrothion. Adrenal hyperfunction manifesting as increased organ weight and elevated plasma corticosterone level was noted along with strong cholinergic signs in rats which received 30 mg/kg bw of fenitrothion. At lower doses such as 3 or 0.3 mg/kg bw of fenitrothion, rats had no strong cholinergic signs, adrenal hyperfunction, or evidence of immunosuppression despite significant suppression of systemic cholinesterase (ChE) activities. In mice, no suppression of SRBC-PFC number or mixed lymphocyte reaction was noted even at the highest dose (40 mg/kg bw) of fenitrothion, at which significant suppression of systemic ChE activities but no cholinergic signs were noted. These findings strongly suggest that the immunosuppressive effect of fenitrothion noted in rats was due to systemic, potent cholinergic stress and that fenitrothion has no immunotoxicity in mice and rats.
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PMID:Immunotoxicological insignificance of fenitrothion in mice and rats. 892 43

Accommodation and pupil constriction result from parasympathetic stimulation from the Edinger-Westphal (EW) nucleus of the midbrain resulting in release of acetylcholine at the neuromuscular junctions of the ciliary muscle and iris. Cholinergic and adrenergic drugs can be applied topically to evaluate the effects on the pupil and accommodative system without input from the EW nucleus. This study is directed at characterizing how topical low dose echothiophate, an anti-cholinesterase inhibitor (i.e., an indirect cholinergic agonist), epinephrine, an adrenergic agonist, and timolol maleate, a beta adrenergic antagonist, affect pupil diameter, resting refraction and accommodative amplitude and dynamics in rhesus monkeys. The effects of 0.015% echothiophate, 2% epinephrine, 0.5% timolol maleate and saline on pupil diameter and resting refraction were measured in one eye each of four normal rhesus monkeys for 60-90 min following topical instillation. Pupil diameter was measured with infrared videography and refraction was measured with a Hartinger coincidence refractometer. Effects on static and dynamic EW stimulated accommodation were studied in three iridectomized monkeys (ages 5, 6 and 12 years) with permanent indwelling stimulating electrodes in the EW nucleus. Dynamic accommodative responses were measured with infrared photorefraction for increasing current amplitudes before and during the course of action of the pharmacological agents. Echothiophate caused a significant decrease in pupil diameter of 3.07 +/- 0.65 mm (mean +/- SEM, p < 0.01), and a myopic shift in resting refraction of 1.30 +/- 0.39 D (p < 0.05) 90 min after instillation. Epinephrine caused a 2.76 +/- 0.38 mm (p < 0.01) increase in pupil diameter with no change in resting refraction 60 min after instillation. Timolol maleate resulted in no significant change in either pupil diameter or resting refraction 60 min after instillation. There was no significant change in maximum EW stimulated accommodative amplitude after any agent tested. The amplitude vs. peak velocity relationship for accommodation was significantly different after echothiophate and timolol maleate, and for disaccommodation after echothiophate, epinephrine and timolol maleate. In conclusion, when tested objectively in anesthetized monkeys, epinephrine and timolol maleate did not alter resting refraction or accommodative amplitude, but did have small, significant affects on accommodative dynamics. This suggests that there is an adrenergic component to the accommodative system. Low dose echothiophate had significant effects on pupil diameter and resting refraction, with only small effects on the dynamics of the accommodative response.
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PMID:Autonomic drugs and the accommodative system in rhesus monkeys. 1978 72