Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 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

Light microscopic observations using Nomarski optics on the aldehyde-fixed hypothalamus of normal adult cats, monkeys and rabbits revealed the presence of cells in the supraoptic, paraventricular and periventricular nuclei which possessed yellow birefringent inclusions. Immunogold labelling showed that in each species the cells displayed oxytocin-like immunoreactivity, both in electron-dense inclusions within some (but not all) cisterns of rough endoplasmic reticulum and in secretory granules. The cells in cats and rabbits were in all respects indistinguishable from the homologous 'birefringent' cells previously described in rats, but in monkeys, cells frequently contained additional inclusions in cisterns of rough endoplasmic reticulum which did not display oxytocin or vasopressin-like immunoreactivity, even after trypsin, pepsin or chymotrypsin treatment of sections. Observations on cats and rabbits using fluorescence microscopy revealed that the birefringent cells possessed bright autofluorescence which facilitated the identification of more cells than were seen using Nomarski optics alone. Autofluorescence was abolished when sections were mounted in glycerol, or when exposed to light for protracted periods of time. Attempts to label for monoamines in these cells were not successful, suggesting that the fluorescence is not due to aldehyde-induced amine fluorescence. It is not clear why neuropeptides are retained in some rough endoplasmic reticulum cisterns. It is possible that these birefringent cells contain a peptide, or peptides, which are abnormal in some manner, or which may be other members of the oxytocin gene family. Alternatively, the processing of neuropeptides to permit their export to the Golgi apparatus may be deficient. Acetylcholinesterase (AChE) histochemistry revealed that, unlike other oxytocin neurons, cells with intracellular accretions lacked detectable acetyl cholinesterase. As AChE is a known peptidase, it may be involved in regulating peptide export from the rough endoplasmic reticulum.
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PMID:Neuropeptide accretions in the endoplasmic reticulum of oxytocinergic neurons in cats, monkeys and rabbits: a widespread phenomenon. 129 66

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

Several cholinergic processes were demonstrated and partially characterized in rabbit kidney cortical minces: choline uptake, acetylcholine synthesis and calcium-dependent release. Minces took up labelled choline, acetylated it, and stored it in a pool that was not readily accessible to physostigmine-sensitive cholinesterase activity. [3H]Acetylcholine synthesis but not [3H]choline uptake was inhibited by the removal of sodium ions or incubation at 0 degrees C. The release of newly synthesized [3H]acetylcholine was increased by 300 mOsmol urea in a calcium-dependent manner, but not by potassium depolarization (300 mOsmol), vasopressin (10 microM), or bradykinin (10 microM). These results suggest that acetylcholine may be synthesized by non-neuronal rabbit kidney cortical cells and that this transmitter may be released in response to physiological levels of urea.
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PMID:Synthesis and release of acetylcholine in the rabbit kidney cortex. 143 79

Effect of vasopressin, oxytocin and LHRH (10 and 20 pg/ml medium) on the proliferation and metabolism of cultured rat bone marrow stromal cells was investigated by methyl-3H-thymidine incorporation, cytochemistry and estimation of enzyme activities. Vasopressin did not change of the activity of tetrahydrofolate dehydrogenase (4HFDH), lactate dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G6PD) and the level of reduced glutathione (GSH). However, the higher concentration of vasopressin significantly lowered the activity of acetylcholinesterase (AchE). As compared with the control cultures, stromal cells grown in the presence of oxytocin showed higher (at lower hormone concentration) and lower (at higher concentration) LDH activity as well as lower G6PD activity (only at higher concentration), while the activity of AchE and the level of GSH was not changed. LHRH significantly increased G6PD and AchE activity and decreased LDH activity in the cultured cells. As revealed by cytochemistry, LHRH specifically enhanced 4HFDH activity in reticular cells.
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PMID:Effect of vasopressin, oxytocin and LHRH on the proliferation and metabolism of rat bone marrow stromal cells in culture. 176 8

It was found that acetylcholine (ACh) at the concentration of 10(-3) M inhibited ADH-stimulated water transport through the wall of amphibian urinary bladder. This effect was suggested to be caused by an interaction of ACh with acetylcholinesterase (AChE) rather than by a stimulation of the M- or N-cholinoreceptor. The inhibitory action of ACh was completely suppressed in the presence of various AChE inhibitors (physostigmine, proserine, armine, Gd-42, acridine-iodmethylate), while an inhibitor of butyrylcholinesterase (BuChE), AD-4, failed to affect it. In accord with this observation the activity of AChE (but not of BuChE) was demonstrated in the urinary bladder epithelium. Since, in addition to the hydrosmotic effects of pituitrine, 8-arginine-vasopressin or oxytocin, ACh blocked also effects of forskolin or cyclic AMP, one may conclude that it acts at some post-cyclic AMP production stage. AChE-dependent inhibition of the ADH-stimulated water transport decreased significantly when the serosal pH was raising from 7.2 to 8.0, but was augmented by serosal acidification (pH 6.8), whereas such pH alterations did not affect the activity of the epithelium AChE. The effect of ACh under consideration was suppressed by adding amiloride (10(-4) M) to the serosal solution. Similarly, the ACh effect was blocked by an inhibitor of Ca-dependent K+ channels, 4-aminopyrdine, which in addition prevented the inhibition of the ADH-stimulated water transport by the serosal acidification. It was noteworthy that some other K+ channel blockers (Ba2+, Cs+, tetraethylammonium, apamine, quinine) did not affect either the water transport or the antipituitrine effect of ACh. In conclusion, we suggest that the inhibitory action of ACh on the ADH-stimulated water transport in the urinary bladder is mediated through the intracellular acidification resulting from ACh interaction with AChE. It is unlikely that the acidification is merely a consequence of the ACh hydrolysis, rather the ACh-AChE interaction induces directly an increase in the proton conductivity of the basolateral membrane of the urinary bladder epithelium.
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PMID:[Acetylcholinesterase and the ADH-dependent transport of water in the amphibian bladder]. 181 71

Acetylcholinesterase activity was demonstrated histochemically at light- and electron-microscopic levels, in Vibratome sections of the supraoptic nucleus of fixed hypothalami derived from osmotically stimulated and unstimulated Long Evans rats, from homozygous Brattleboro rats with hypothalamic diabetes insipidus, from lactating rats, from normal adult male house mice (Mus musculus) and from mice with hereditary nephrogenic diabetes insipidus (di/di). Reaction product was located in supraoptic magnocellular neurons; in dorsal and rostral aspects of the supraoptic nuclei lightly stained cells predominate, whereas in ventral and caudal regions densely staining perikarya predominate. Pre- and post-embedding immunocytochemical detection of oxytocin-neurophysin or vasopressin-neurophysin, combined with acetylcholinesterase histochemistry, showed that the lightly staining cells are oxytocinergic, and the densely staining cells vasopressinergic. Osmotic stimulation of the animals, either by substitution of drinking water for 3 days with 2.5% saline or reason of genetic defects which result in diabetes insipidus, enhanced the acetylcholinesterase activity of the vasopressin neurons but had little effect on the weekly acetylcholinesterase-reactive oxytocin cells. Acetylcholinesterase activity was particularly marked in the hypertrophied abnormal magnocellular neurons of homozygous Brattleboro rats which do not release significant amounts of vasopressin. The increased acetylcholinesterase activity in osmotically stimulated animals cannot, therefore, be a function of vasopressin. Acetylcholinesterase activity was also detected in large multipolar neurons lying dorsolateral to the supraoptic nucleus, and in their fine axonal processes which project towards the supraoptic nucleus. A very few synaptic boutons surrounded by acetylcholinesterase reaction product were found in contact with magnocellular neuron basal dendrites. However, much of the punctate acetylcholinesterase reactivity observed at the light microscopic level and previously interpreted as representing the loci of cholinergic synaptic boutons was shown to be intracellular, and probably caused by acetylcholinesterase activity in some large, secondary lysosomes.
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PMID:Differential distribution of acetylcholinesterase activity among vasopressin- and oxytocin-containing supraoptic magnocellular neurons. 276 86

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

The laterodorsal tegmental nucleus (ntdl) contains a cluster of cells located just medial to the locus coeruleus in the pontine brainstem. The ntdl has been shown to project both rostrally to the forebrain and diencephalon and caudally to the spinal cord. In an effort to characterize this region neurochemically, the present study was conducted to identify a variety of neurochemicals localized within perikarya and fibers of the ntdl and surrounding nuclei. Rats were perfused with formalin, and brain sections were processed for fluorescence immunocytochemistry and acetylcholinesterase (AChE). Of the neurochemicals screened, atrial natriuretic factor (ANF), choline acetyltransferase (ChAT), cholecystokinin (CCK), calcitonin gene-related peptide (CGRP), dynorphin B (Dyn B), galanin, somatostatin, substance P, neurotensin (NT), neuropeptide Y (NPY), vasopressin, vasoactive intestinal polypeptide (VIP), serotonin (5HT), glutamic acid decarboxylase (GAD), and tyrosine hydroxylase (TH) were studied. AChE and ChAT staining revealed that the ntdl contains mostly cholinergic neurons. In addition, brightly reactive substance P and galanin and paler staining CRF, ANF, CGRP, NT, VIP, and Dyn B cell bodies were found within the ntdl. Varicose fibers in this nucleus also contained these peptides in addition to CCK, GAD, TH, 5HT, and NPY. The dorsal tegmental nucleus, dorsal raphe nucleus, locus coeruleus, and the parabrachial region contained a dense and varied assortment of peptides with distinct positions and patterns. This multiplicity of neurochemicals within this area suggests a possible influence on a variety of functions modulated by the ntdl and other closely associated tegmental nuclei.
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PMID:Immunocytochemical localization of peptides and other neurochemicals in the rat laterodorsal tegmental nucleus and adjacent area. 289 81

Recent electrophysiological experiments have suggested that electrical stimulation of an area dorsolateral to the rat supraoptic nucleus (SON) activates a cholinergic pathway to the vasopressin neurons of the SON. As no detailed information is available concerning the distribution and projections of the cholinergic neurons in this area, we have sought to provide this using a combination of choline acetyltransferase (ChAT) immunocytochemistry and acetylcholinesterase (AChE) histochemistry. In some cases, these techniques were applied to the same neurons. Almost all neurons just outside of the SON that showed ChAT-like immunoreactivity also stained densely for AChE. These cells were distributed in a region dorsolateral to the SON. Light, punctate AChE staining around SON neurons was observed predominantly in the more ventral and posterior parts of the nucleus and were suggestive of synaptic terminals. Cholinergic fibres were found to enter the SON mainly from a lateral direction, turning in an anterior or posterior direction inside the nucleus. These results support the conclusion of earlier studies that the major cholinergic input to the SON arises in its immediate vicinity. We hypothesize that these ChAT/AChE-positive neurons are those responsible for cholinergically mediated, osmotically-stimulated release of vasopressin.
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PMID:Mapping of cholinergic neurons associated with rat supraoptic nucleus: combined immunocytochemical and histochemical identification. 636 54


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