Publications by authors named "Sumners C"

The cellular characteristics of the beta-adrenoreceptor in glial and neuronal cells from the newborn rat brain were determined by (-)-[125I]iodocyanopindolol binding. In membranes from both cell types, the binding was saturable and from competition assays the potency series of (-)-isoproterenol greater than (-)-epinephrine = (-)-norepinephrine greater than (+)-isoproterenol was observed. 5'-Guanylyl-imidodiphosphate reduced the affinity of (-)-isoproterenol for the beta-adrenoreceptor from glial cells but had no effect on agonist affinity in neuronal cells.

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The effect of chronic administration of deoxycorticosterone acetate (DOCA) on the regulation of angiotensin II (AII) receptors in the brains of adult rats was compared with their drinking and pressor responsiveness to both peripheral and central administration of AII. Analysis of AII receptor binding in a block of tissue containing the hypothalamus, thalamus and septum (HTS) after treatment for 8 weeks with DOCA-salt (240 micrograms/kg/day) revealed a significant increase in the number of AII-binding sites compared to salt-loaded controls (Bmax 9.65 vs 6.

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The expression of alpha 1-adrenergic receptors and norepinephrine (NE)-stimulated hydrolysis of inositol phospholipid has been studied in neuronal cultures from the brains of normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SH) rats. Binding of 125I-2-[beta-(4-hydroxyphenyl)-ethyl-aminomethyl] tetralone (HEAT) to neuronal membranes was 68-85% specific and was rapid. Competition-inhibition experiments with various agonists and antagonists suggested that 125I-HEAT bound selectively to alpha 1-adrenergic receptors.

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Neuronal cultures from one-day-old brains of Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats were used to determine the effect of sodium ions on angiotensin II (Ang II) receptors in order to understand the mechanism of action of sodium at the cellular level. Incubation with sodium chloride of neuronal cultures from WKY rats caused a rapid and dose-dependent increase in the specific binding of 125I-Ang II to its receptors. A 260% increase in the binding was observed with 150 mM NaCl.

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In this study we have characterized the uptake of [3H]norepinephrine (NE) into neuronal co-cultures of rat hypothalamus and brain stem and have examined the effects of angiotensin II (ANG II) on this uptake. Neuronal co-cultures prepared from the brains of 1-day-old Sprague-Dawley (SD) or Wistar-Kyoto (WKY) rats exhibited sodium-dependent and sodium-independent portions of the total [3H]NE uptake. The sodium-dependent uptake was abolished by blockers such as maprotiline, desmethylimipramine, and xylamine (0.

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Epinephrine and norepinephrine together (E + NE) and epinephrine (E) alone were infused intravenously in stepwise increasing doses during progressive isotonic tetanic contractions. The goal was to mimic, for in situ dog skeletal muscle, the concentrations of these catecholamines in the blood and the contractions during progressive exercise. The concentrations of lactate and O2 in arterial and muscle venous blood, the arterial plasma concentration of E and NE, PO2 in arterial and muscle venous blood, and the venous outflow were measured.

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Chronic administration of two doses of estradiol benzoate (30 and 46 micrograms/kg/day) reduced the drinking response to acute administration of either isoproterenol (25 micrograms/kg, s.c.), the beta-adrenergic agonist, or angiotensin II (Ang II) (200 micrograms/kg, s.

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Uptake of [3H]norepinephrine (NE) has been characterized and compared in neuronal cultures prepared from the brains of 1-day-old normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SH) rats. In cultures from both strains total [3H]NE uptake consisted of a sodium-dependent portion and a sodium-independent portion. The sodium-dependent [3H]NE uptake was inhibited by NE uptake blockers such as maprotiline or desmethylimipramine (both at 0.

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Binding of 125I-angiotensin II (ANG II) to neuronal cultures made from the brains of 1-day-old normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SH) rats was time dependent, saturable, reversible, and 90-95% specific. Neuronal cultures from SH rats bound 50-70% more 125I-ANG II compared with their WKY controls. Scatchard analysis revealed that the increase in the specific binding of ANG II to SH rat neuronal cultures was due to an increase in the number of binding sites per cell rather than change in the affinity of receptors for ANG II.

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This study was designed to test the hypothesis that epinephrine (E) and norepinephrine (NE) increase net muscle lactate output (L) of in situ gastrocnemius-plantaris muscle group during contractions. Plasma [E] and [NE] were measured before and after the surgical isolation of the muscle and at 10-min intervals during the 60-min experiments. Plasma [E] and [NE] were increased threefold by intravenous infusions of E (n = 3) or NE (n = 3) at a rate of 1.

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Primary neuronal cultures from 1-day-old rat brains, which contain angiotensin II (ANG II) immunoreactivity within the neurons and are capable of de novo synthesis of this immunoreactivity, have been used in this study to determine the nature of this immunoreactivity by high-performance liquid chromatography (HPLC). Neuronal cultures from the brains of normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats were found to contain ANG II immunoreactivity, which co-migrated with authentic ANG II on HPLC. The angiotensin detected in brain cultures was not derived from the growth medium, and its level was significantly decreased by incubating the cultures with captopril.

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Neuron-enriched primary cultures from 1-day-old rat brains have been used to study the influence of catecholamines on angiotension II receptors. Treatment of cultures with alpha-methyl-p-tyrosine caused a time- and concentration-dependent increase in the specific binding of 125I-angiotensin II and a decrease in neuronal norepinephrine and dopamine contents. A maximum increase of 75% in the binding and a decrease of 67% in catecholamine content was observed with 400 microM alpha-methyl-p-tyrosine.

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Several dopamine (DA) receptor agonists, notably N,N-dipropyl-2-aminotetralin analogues differing in the number and position of phenolic hydroxyl groups, were evaluated in model systems for pre- and postsynaptic dopaminergic activity. Apomorphine, piribedil and pergolide were included for comparison. All compounds inhibited the gamma-butyrolactone (GBL)-induced increase in DA concentrations in the rat striatum and olfactory tubercle, although a dose-dependency could not be demonstrated for one of the compounds, i.

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Interactions between norepinephrine and angiotensin II were investigated in neuron-enriched primary brain cell cultures, which have been demonstrated to contain catecholamines, angiotensin II-like immunoreactivity and specific receptors for angiotensin II. Angiotensin II (7.5 and 15.

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Catecholamines have been visualized and quantified in primary cultures of whole rat brain. Twenty-one-day old cultures treated with glyoxylic acid and viewed under a fluorescence microscope revealed neurons stained specifically with blue-green catecholamine fluorescence. Brightly stained multipolar cell bodies were seen, along with stained neurites and varicosities, and there was no staining associated with the non-neuronal portion of the culture.

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Centrally injected angiotensin II (ANG II) produces a pressor response. The effect of ANG II injected intracerebroventricularly on catecholamine utilization in specific rat brain regions was examined. A pressor dose of ANG II stimulated an increase in norepinephrine (NE) utilization in the locus coeruleus, raphe magnus and AI regions of the brain stem, and in the hypothalamus.

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The effects of neurotensin upon blood pressure in conscious rats were examined after intracerebroventricular (i.v.t.

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The dopaminergic actions of five hydroxylated dopamine analogues have been examined for: i) Ability to induce stereotypy, ii) Effects upon dopamine metabolism, iii) Ability to antagonise the rise in striatal dopamine caused by gammabutyrolactone. With the exception of the resorcinol derivative 2-(3,5-dihydroxyphenyl)-N,N-dipropylethylamine, all of the compounds tested exhibited dopamine-like actions, and similarities were found in the induction of stereotypy and in the reduction of dopamine metabolism. For example, 2-(3-hydroxyphenyl)-N,N-dipropylethylamine had a short duration of action as far as reducing dopamine metabolism and inducing stereotypy were concerned.

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The dopaminergic prodrug dibenzoyl-6,7-ADTN (DB-6,7-ADTN) can enter the brain following intraperitoneal injection and be hydrolysed to produce low concentrations of the dopamine agonist 6,7-ADTN. Intraperitoneal injections of DB-6,7-ADTN produce a decrease in motor activity and in the present study this response has been characterised, and the underlying mechanisms examined. Doses of 10-100 mumol/kg DB-6,7-ADTN elicit a strong hypomotive response, which is dose dependent.

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A study was made of the effects of manipulating brain dopaminergic activity upon drinking induced by intracerebroventricular administration of angiotensin II or carbachol. Non-specific lesions induced by injecting 6-hydroxydopamine (6-OHDA) into the cerebroventricles caused a significant reduction in angiotensin-induced thirst without affecting carbachol drinking. specific 6-OHDA-induced lesions of the dopaminergic nigro-striatal pathway also attenuated the angiotensin-induced response, while unilateral lesions reduced and bilateral lesions almost completely abolished the effect.

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The effect of a series of neuroleptic drugs on the drinking response elicited by intracerebroventricular injection of either angiotensin or carbachol into conscious rats was studied. The i.p.

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