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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 771 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of selective inhibition of monoamine oxidase (MAO) subtypes A and B on striatal metabolism of DOPA to dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid; HVA) was studied in halothane-anesthetized rats 3 weeks after unilateral 6-hydroxydopamine lesion of the substantia nigra. Implantation of bilateral microdialysis probes allowed simultaneous quantitation of metabolite production on lesioned and control sides. The DOPA was administered as a 15-min bolus of 1 mM solution in the striatal microdialysate. Rats were pretreated with the selective MAO-A inhibitor clorgyline, or the selective MAO-B inhibitors deprenyl or TVP-101 [2,3-dihydro-N-2-propynyl-1H-inden-1-amine-(1R)-hydrochloride]. Intrastriatal infusion of DOPA caused an increased efflux of DA, DOPAC, and HVA, which was greater on the intact side. Clorgyline, but not deprenyl or TVP-101, increased post-DOPA DA efflux on both intact and lesioned sides. Clorgyline also caused a marked suppression of post-DOPA DOPAC and HVA effluxes, whereas only mild effects were produced by the MAO-B inhibitors. There was no evidence for a differential effect of MAO-B inhibition on efflux of DA or metabolites in the lesioned as compared with the control striatum. The results indicate a major role for MAO-A in DA metabolism both intra- and extraneuronally in the rat striatum.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The pituitary-adrenocortical, sympathoadrenomedullary and renin-angiotensin-aldosterone systems contribute to circulatory and metabolic homeostasis during stress. One possible site of co-ordination of these systems is the β-adrenoceptor.2. To determine whether circulating β-adrenoceptor agonists can act hormonally to stimulate these systems simultaneously, plasma concentrations of corticotrophin (ACTH), noradrenaline, adrenaline and plasma renin activity were measured during graded intravenous infusions of isoprenaline in 20 people.3. Administration of isoprenaline caused dose-related increases in noradrenaline (94% at the highest dose) and renin activity (189%), but decreases in ACTH (25%) and adrenaline (20%), findings inconsistent with simultaneous activation of these systems by circulating β-adrenoceptor agonists.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 21 (1992), S. 0 
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ionizing radiation (IR) irreversibly damages salivary glands. The pathologic mechanism is unknown. Previously we reported that parotid serous acinar cells may not be the primary site of damage by IR. The purpose of this study was to determine if IR alters sympathetic nerve function in rat parotid glands. Male adult rats received a single dose of radiation (20 Gy) to the head and neck. Three days after IR, parotid saliva secretion induced by norepinephrine (NE) was completely blocked. Catecholamine uptake and metabolism were studied by injecting [3H] dopamine ([3H]DA) into irradiated rats, as a bolus. After 60 min, animals were sacrificed and the parotid gland, submandibular gland, and left ventricle removed. Tissue contents of [3H]DA and [3H]NE, identified by HPLC, were unaffected by IR. The results indicate that IR abolishes acinar responsiveness to NE without affecting parotid sympathetic nerve function.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 298-305 
    ISSN: 1432-1912
    Keywords: Norepinephrine ; Synapse ; Neuroeffector junction ; Sympathetic nervous system ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We estimated vascular neuroeffector junctional norepinephrine concentrations and their relation to pressor responses by measuring plasma norepinephrine levels and blood pressure during sympathetic stimulation or norepinephrine infusion in pithed, vagotomized, α2-adrenoceptor blocked, adrenal-demedullated rats with and without uptake1 blockade by desipramine. For an increment in mean arterial pressure of 50 mm Hg, the estimated mean junctional norepinephrine concentration (ES 50m) was about 7 nmol/l. Norepinephrine concentration gradients between the site of norepinephrine release and plasma appeared to be equal and reciprocal for sympathetic stimulation and for norepinephrine infusion. These gradients were reduced equally (by about two-thirds) after desipramine treatment, indicating that removal of both released and infused norepinephrine is mainly by neuronal uptake.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 500-505 
    ISSN: 1432-1912
    Keywords: Clorgyline ; Microdialysis ; Yohimbine ; α2-Adrenoceptors ; Tetrodotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chronic but not acute treatment of rats with MAO inhibitory, as with other antidepressant drugs, has been shown to down-regulate the number of cerebro-cortical ß-adrenoceptors. In order to establish whether this effect is associated with an increase in cortical noradrenaline release, rats were treated for 1, 3 or 21 days with clorgyline (2 mg/kg i.p. single injection; 1 mg/kg i.p. repeated injections), and the frontal cortex was then perfused by microdialysis in the awake animal. Control animals were injected with saline. The concentration of noradrenaline in the microdialysate increased only slightly after 1 or 3 days of clorgyline treatment but increased fourfold over control levels after 21 days treatment. Yohimbine (20 μmol/1) added to the perfusing solution caused a similar degree of enhancement in microdialysate noradrenaline concentration in all groups of rats. Tetrodotoxin (10 μmol/1) reduced noradrenaline concentration to low levels in all groups of animals, but noradrenaline was still detectable in the microdialysate in rats treated with clorgyline for 21 days. Concentrations of the deaminated metabolites dihydroxyphenylacetic acid, dihydroxyphenylglycol and methoxy-hydroxyphenylglycol were lowest after the 21 day clorgyline treatment. Determination of enzyme activity ex vivo showed that MAO-A was inhibited more than 95% by all clorgyline treatments with less than 10% inhibition of MAO-B. The results indicate that cerebrocortical noradrenaline release increases gradually during chronic MAO inhibition. This may be the result of more complete inhibition of the enzyme with time, not detectable by the ex vivo assay, but shown by the progressive reduction in metabolite levels. The intraneuronal consequence of this effect could be increased vesicular packaging of noradrenaline, together with reduction in net uptake from the synaptic cleft because of increased axoplasmatic noradrenaline levels. Modification of neuronal firing rate may also play a role in the net change in cortical noradrenaline release. The increase in extracellular fluid noradrenaline concentration occurs over a time period similar to that required for ß-adrenoceptor down-regulation, and for the onset of clinical antidepressant action.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of inherited metabolic disease 16 (1993), S. 907-908 
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Applied psychophysiology and biofeedback 2 (1977), S. 93-105 
    ISSN: 1573-3270
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Sympathetic adrenergic nervous activity during operantly conditioned hypertension was evaluated by assessing the effects of specific alpha-(phentolamine or phenoxybenzamine) and beta- (propranolol) adrenergic blockers in baboons reinforced for increasing diastolic pressure in daily, 12-h sessions. In the first 10 min of control (no blockade) sessions, mean heart rate increased 24 bpm (21%) above the value for the 10 min immediately prior to the beginning of the sessions; systolic pressure increased 27 mm Hg (22%) and diastolic pressure increased 24 mm Hg (31%). Betablockade eliminated the tachycardia but did not attenuate the increased blood pressure. Alpha-blockade did not attenuate the increased blood pressure significantly either. Combined alpha- and beta-blockade did significantly attenuate the increase in diastolic pressure, but consistent, significant increases in systolic pressure (17 mm Hg, 17%) and diastolic pressure (16 mm Hg, 26%) still occurred. The results support the participation of the sympathetic adrenergic nervous system in producing operantly conditioned blood pressure changes, but the results are also consistent with the additional participation of nonadrenergic factors in operantly conditioned hypertension.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Applied psychophysiology and biofeedback 2 (1977), S. 127-138 
    ISSN: 1573-3270
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Baroreflex sensitivity was measured in baboons operantly conditioned to increase their diastolic blood pressure in daily, 12-hr sessions, by using the extent of increases in interpulse interval per unit of increase in systolic pressure after intravenous phenylephrine injection as an index of baroreflex sensitivity. Following training, baroreflex sensitivity increases averaging 32% were observed before and after the 12-hr conditioning sessions. During the conditioning sessions, however, consistent diastolic blood pressure elevations averaging 17% (14 mmHg) were accompanied by significant decreases in baroreflex sensitivity averaging 44% relative to the increased “before” and “after” sensitivity levels. The results suggest that changes in baroreflex sensitivity participate in operantly conditioned blood pressure changes.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1619-1560
    Keywords: stress ; sympathetic nervous system ; catecholamines ; parasympathetic nervous system ; heart rate ; spectral analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Overstimulation of sympathetic nervous system activity is related to atherosclerotic cardiovascular disease risk, but the role of parasympathetic activity in this association is not clear. This study evaluated sympathetic and parasympathetic function by spectral analysis of heart rate variability and plasma levels of norepinephrine (NE) epinephrine (EPI), dihydroxyphenylglycol (DHPG), dihydroxyphenylalanine (DOPA) and dihydroxyphenylacetic acid (DOPAC). It also examined the interrelationships among these parameters and established atherosclerotic cardiovascular disease risk factors in 53 men (mean age 59.5 years). During supine rest, low-frequency power correlated positively with high-frequency power (r = 0.58, p 〈 0.001), plasma NE correlated with plasma DHPG (r = 0.41, p 〈 0.001) and plasma DOPA with DOPAC (r = 0.47, p 〈 0.001) but neither low- nor high-frequency power was correlated with plasma levels of any catechol. Among risk factors, plasma NE correlated with fasting insulin and mean arterial blood pressure, and urine NE correlated with body mass index. Both low- and high-frequency power correlated positively with insulin levels. Orthostasis decreased high-frequency power and increased low-frequency power and plasma NE levels. During the oral glucose tolerance test, both high- and low-frequency power increased, plasma NE levels were unchanged, and plasma EPI levels decreased [88.5 ± 18 (SEM) versus 52.5 ± 12 pM,p = 0.001]. The results suggest that orthostasis decreases and the oral glucose tolerance test increases parasympathetic outflows, whereas both stimuli increase sympathetic outflows. Among all atherosclerotic cardiovascular disease risk factors, hyperinsulinaemia showed the strongest association with autonomic nervous system activity, especially parasympathetic activity. Estimates of sympathetic responses obtained from power spectral analysis of heart rate variability agree poorly with those from plasma levels of catechols, possibly because of a parasympathetic contribution to low-frequency power and independence of sympathoneural outflows to the arm and heart.
    Type of Medium: Electronic Resource
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