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  • 1
    Electronic Resource
    Electronic Resource
    Release by Electrical Stimulation of Endogenous Glutamate, γ-Aminobutyric Acid, and Other Amino Acids from Slices of the Rat Medulla Oblongata (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Evidence was obtained for the release of amino acids by electrical stimulation of slices of regions of the rat medulla oblongata: rostral ventrolateral, caudal ventrolateral, and caudal dorsomedial. There was a Ca2+-dependent, tetrodotoxin-sensitive increase in the efflux of aspartate, glutamate, γ-aminobutyric acid (GABA), glycine, and β-alanine in all regions examined. There were distinct regional differences in the relative amounts of amino acids released. These results provide evidence for the possible neurotransmitter role of aspartate, glutamate, GABA, glycine, and β-alanine in these regions of the rat medulla oblongata.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb10926.x
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  • 2
    Electronic Resource
    Electronic Resource
    Aspartate Aminotransferase for Synthesis of Transmitter Glutamate in the Medulla Oblongata: Effect of Aminooxyacetic Acid and 2-Oxoglutarate (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract The effects of aminooxyacetic acid (AOAA), a transaminase inhibitor, and 2-oxoglutarate, a precursor to glutamate by the activity of aspartate aminotransferase (AAT), on slices of rat medulla oblongata, cerebellum, cerebral cortex, and hippocampus were studied. The slices were superfused and electrically stimulated. There was a Ca2+-dependent stimulus-evoked release of endogenous glutamate, γ-aminobutyric acid (GABA), and β-alanine in all regions examined. AOAA (10-4 and 10-3M) decreased the release of glutamate in the medulla oblongata and cerebellum but not in the hippocampus. l-Canaline, a specific inhibitor of ornithine aminotransferase, did not affect the glutamate release in the medulla. 2-Oxoglutarate (10-3M) increased the release of glutamate in the medulla oblongata and cerebellum but not in the cerebral cortex and hippocampus. Treatment with AOAA (10-4M) almost abolished the activities of AAT in all regions studied. AOAA (10-4 and 10-3M) increased the stimulus-evoked release of GABA in the cerebellum, cerebral cortex, and hippocampus, whereas the stimulus-evoked release of β-alanine was decreased by this agent in all regions studied. These results suggest the participation of AAT in the synthesis of the transmitter glutamate in the medulla oblongata and cerebellum of the rat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb01857.x
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  • 3
    Electronic Resource
    Electronic Resource
    Altered Mitogen-Activated Protein Kinase Activation In Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats (2002)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 29 (2002), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We previously reported that activation function of mitogen-activated protein kinases (MAPK) is enhanced in aorta strips from both prehypertensive and hypertensive spontaneously hypertensive rats (SHR) and that this enhancement of MAPK activation results from enhanced MAPK activation reactivity to angiotensin (Ang) II in SHR aorta strips.2. The purpose of the present study was to examine whether the enhanced function of the vascular angiotensin system observed in SHR aorta strips results from genetic alterations of vascular smooth muscle cells from SHR.3. Basal MAPK activity was within normal limits in cells from 4-week-old SHR, whereas enzyme activity was enhanced in 9-week-old SHR compared with age-matched Wistar-Kyoto (WKY) rats.4. Mitogen-activated protein kinase activation reactivity to AngII and endothelin-1 was enhanced in 9-week-old SHR cells but not in 4-week-old SHR cells. The enhancement of basal MAPK activity in 9-week-old SHR cells was abolished by a combination of the angiotensin AT1 receptor antagonist losartan and the endothelin receptor antagonist BQ123.5. These findings suggest that MAPK activation function in 4-week-old SHR cells is not enhanced. Thus, it appears that factors outside vascular smooth muscle cells are needed for the enhanced MAPK activation observed in 4-week-old SHR aorta strips. In 9-week-old SHR, MAPK activation function is enhanced in cells themselves and this function may, at least in part, contribute to the enhanced MAPK activation observed in SHR aorta strips.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03694.x
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  • 4
    Electronic Resource
    Electronic Resource
    ACETYLCHOLINE RELEASE IN THE ROSTRAL VENTROLATERAL MEDULLA OF SPONTANEOUSLY HYPERTENSIVE RATS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Central acetylcholine (ACh) has been implicated in the pathogenesis of experimental hypertension and the rostral ventrolateral medulla (RVLM) is an important area for cardiovascular regulation. The purpose of this study was to determine whether cholinergic neurotransmission in the RVLM is altered in spontaneously hypertensive rats (SHR).2. Experiments were performed on male SHR (12–16 weeks) and age-matched Wistar-Kyoto rats (WKY). The rats anaesthetized with pentobarbital were placed in a stereotaxic apparatus. For determining the release of ACh in the RVLM, a dialysis probe was introduced into the RVLM.3. An RVLM microinjection of cholinergic agents elicited an increase in blood pressure. The pressor response to physostigmine was greater in SHR than that of WKY whereas there was no difference in the pressor response to ACh or carbachol between SHR and WKY.4. The release of ACh in the RVLM was greater in SHR than that of WKY. Physostigmine (0.5 mg/kg, i.p.) produced increases in medulla ACh contents. The increase in ACh content of the rostroventral medulla including the RVLM was greater in SHR than that of WKY whereas there was no difference in ACh contents of the other three parts of the medulla oblongata between SHR and WKY.5. Depressor responses to scopolamine injected bilaterally into the RVLM were greater in SHR than those of WKY.6. These results suggest that ACh release is enhanced specifically in the RVLM of SHR. It appears that this enhanced release of ACh in the RVLM of SHR contributes to the maintenance of hypertension in SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02963.x
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  • 5
    Electronic Resource
    Electronic Resource
    Basal transcriptional regulation of rat AT1 angiotensin II receptor gene expression (2004)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 31 (2004), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Angiotensin II AT1A receptors are thought to play an important role in the development of hypertension. The transcriptional factor Sp1 is a ubiquitous transcriptional factor associated with GC-rich promoters and involved in basal promoter activity.2. To examine basal transcriptional levels regulation of the rat AT1A receptor gene, we determined whether two GC-box-related regions within 100 bp of the rat AT1A receptor gene promoter are involved in the basal expression of the gene in A10 cells, a vascular smooth muscle cell line.3. The electrophoretic mobility shift assay demonstrated that incubation of the −98/−79 region and −58/−34 region sequence oligonucleotides with nuclear extracts of rat hypothalamus, liver and adrenal formed DNA–protein complexes and that the addition of unlabelled oligonucleotides containing the Sp1 consensus sequence blocked the formation of the DNA–protein complex. The addition of antibody against Sp1 also blocked the formation of the DNA–protein complex.4. The promoter/luciferase reporter assay demonstrated that the reporter activity of AT1A receptor promoters mutated either within the −98/−79 or the −58/−34 region was lower than that of intact AT1A receptor promoters.5. The promoter activity of AT1A receptor promoters mutated within those two regions was lower than that of promoters mutated within either the −98/−79 or the −58/−34 region.6. These findings suggest that GC-box-regulated sequences within the −98/−79 region and the −58/−34 region are additively involved in basal expression level of the AT1A receptor gene in A10 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.2004.03957.x
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of morphine on release of acetylcholine in the rat striatum: an in vivo microdialysis study (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 9-13 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Morphine ; Dopaminergic system ; In vivo microdialysis ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the effect of morphine on the release of acetylcholine (ACh) in the striatum of freely moving rats using the in vivo microdialysis method. The basal level of ACh was 3.01 ± 0.51 pmol/30 μl/15 min in the presence of neostigmine (10 μM). Tetrodotoxin (1 μM), a selective blocker of voltage-dependent Na+ channels, rapidly decreased the release of ACh in the striatal perfusates. Morphine at a dose of 10 mg/kg (i.p.) caused a reduction of ACh release in the striatum at 90–150 min. However, a lower dose of morphine (5 mg/kg, i.p.) did not affect ACh release in the striatum. The reduction following intraperitoneal administration of morphine was abolished by naloxone (1.0 mg/kg). After microinjection of the neurotoxin 6-hydroxydopamine (6 μg/3 μl, 7 days before) in the substantia nigra, the morphine (10 mg/kg)-induced decrease of ACh was attenuated, and a similar result occurred following reserpine (2 mg/kg, i.p.) 24 h before combined with α-methyl-p-tyrosine (300 mg/kg, i. p.) 2.5 h before. These findings indicate that morphine exerts an inhibitory influence on striatal ACh release in freely moving rats and that this inhibitory effect is mediated by the nigro-striatal dopaminergic system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168765
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  • 7
    Electronic Resource
    Electronic Resource
    Pharmacological characterisation of the α-adrenoceptors responsible for a decrease of blood pressure in the nucleus tractus solitarii of the rat (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 120-125 
    Details
    ISSN: 1432-1912
    Keywords: α-Adrenoceptor agonists ; α-Adrenoceptor antagonists ; Arterial pressure ; Nucleus tractus solitarii
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of various α-adrenoceptor agonists, microinjected into the area of the nucleus tractus solitarii (NTS) at the level of the obex, on blood pressure, and the interaction between noradrenaline and some α-antagonists in the area of the NTS were investigated in anaesthetized male rats. A dose-dependent decrease in blood pressure was induced by noradrenaline. The relative potencies of the substances were adrenaline 〉 noradrenaline 〉 α-methylnor-adrenaline 〉 clonidine 〉 tyramine. In contrast, phenylephrine was ineffective. The hypotensive effect of noradrenaline, α-methylnoradrenaline and clonidine was not affected by pretreatment with 6-hydroxydopamine given intraventricularly, while the effect of tyramine was blocked by the pretreatment. Prior application of phentolamine at the same site antagonized the hypotensive response to noradrenaline. Prazosin was about 10 times less potent than yohimbine in antagonizing the noradrenaline-induced hypotension. The present data suggest that the α-adrenoceptors in the area of the NTS responsible for the decrease in blood pressure are the same type as the peripheral presynaptic α2-adrenoceptors but may be located postsynaptically. It appears that the noradrenergic neurons in the NTS can play a role in blood pressure regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500066
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