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Per-otto Hagen - One of the best experts on this subject based on the ideXlab platform.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. The authors have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and they now report a possible mechanism for this. Binding studies in rabbit aorta with the selective alpha 1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 {plus minus} 4 fmole/10(6) cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in alpha 1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P less than 0.05). This increased affinity for norepinephrine was associated with a greater increase in 32P-labeled phosphatidylinositol (148% intimal thickening versus 76% control) and phosphatidic acid (151% intimal thickening versus 56% control) following norepinephrine stimulation of free floating rings of intimal hyperplastic aorta. These data suggest that the Catecholamine supersensitivity in rabbit aortic intimal hyperplasia is Receptor mediated and may be linked to the phosphatidylinositol cycle.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Abstract Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. We have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and we now report a possible mechanism for this. Binding studies in rabbit aorta with the selective α1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 ± 4 fmole/106 cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in α1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P

Athineos Philippu - One of the best experts on this subject based on the ideXlab platform.

  • Influence of Catecholamine Receptor agonists and antagonists on the ultradian rhythm of the EEG in the posterior hypothalamus.
    Naunyn-Schmiedeberg's archives of pharmacology, 1998
    Co-Authors: Kurt Grass, Helmut Prast, Athineos Philippu
    Abstract:

    The power of delta and theta frequency bands of the EEG in the posterior hypothalamus of the rat fluctuates according to an ultradian rhythm. To investigate, whether Catecholamine Receptor ligands influence the ultradian EEG rhythm, drugs were applied intracerebroventricularly into the lateral ventricle of anaesthetized rats. Injection of the α1-adrenoceptor agonist (±)-methoxamine (150nmol) abolished, while 25nmol of the compound prolonged the cycle duration of the rhythmic changes in the delta and theta frequency bands. Injected into the lateral ventricle, the α2-adrenoceptor agonists 6-ethyl-5,6,7,8-tetrahydro-4H-oxazol[4,5-d] azepin-2-amine (B-HT 933) or clonidine (150nmol each) prolonged the duration of the cycles of both frequency bands. The β1/2-Receptor agonists (±)-orciprenaline (300nmol) and (R)-(–)-isoprenaline (150nmol) slowed down the cycle durations of both frequency bands. The β1-Receptor agonist (±)-xamoterol (300nmol) also prolonged the cycle durations of the delta and theta frequency bands. The β1-Receptor antagonist (S)-(–)-atenolol was ineffective (150 and 300nmol). The β2-Receptor agonist (±)-salbutamol (300nmol) shortened the duration of the ultradian rhythm in the two frequency bands, while the β2-Receptor antagonist (±)-1-[2,3(dihydro-7-methyl-1H-inden-4-yl) oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551) (300nmol) exerted the opposite effect. On the other hand, the D1 Receptor agonist (±)-1-phenyl-2,3,4,5-tetrahydro-1H)-3-benzazepine-7,8-diol (SKF 38393) and the D2 agonist (4aR,8aR)-(–)-quinpirole (150nmol each) slowed down the frequency of the ultradian rhythm. The powers of alpha and beta frequency bands were not significantly influenced by the Catecholamine Receptor ligands used in this study.

  • influence of mediobasal hypothalamic lesion and Catecholamine Receptor antagonists on ultradian rhythm of eeg in the posterior hypothalamus of the rat
    Neuroscience Letters, 1996
    Co-Authors: Kurt Grass, Helmut Prast, Athineos Philippu
    Abstract:

    The delta and theta frequency bands of the EEG in the posterior hypothalamic area (PH) of the urethane-anaesthetized rat vary according to an ultradian rhythm with a frequency of approximately one cycle per 100 min. Injected into the lateral ventricle, prazosin (150 nmol) abolished the rhythmic changes, propranolol (150 nmol) increased, while yohimbine, SKF-83566 and sulpiride (150 nmol each) decreased the cycle duration. Electrocoagulation of the rostral arcuate nucleus and median eminence (Arc-ME) of medial basal hypothalamus abolished the rhythmic EEG changes in the PH. Our results indicate that the ultradian EEG rhythm in the PH is susceptible to regulatory influences mediated by noradrenergic and dopaminergic neurons. For the generation of the ultradian rhythm, the functional integrity of the Arc-ME is required.

O'malley Mk - One of the best experts on this subject based on the ideXlab platform.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. The authors have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and they now report a possible mechanism for this. Binding studies in rabbit aorta with the selective alpha 1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 {plus minus} 4 fmole/10(6) cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in alpha 1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P less than 0.05). This increased affinity for norepinephrine was associated with a greater increase in 32P-labeled phosphatidylinositol (148% intimal thickening versus 76% control) and phosphatidic acid (151% intimal thickening versus 56% control) following norepinephrine stimulation of free floating rings of intimal hyperplastic aorta. These data suggest that the Catecholamine supersensitivity in rabbit aortic intimal hyperplasia is Receptor mediated and may be linked to the phosphatidylinositol cycle.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Abstract Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. We have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and we now report a possible mechanism for this. Binding studies in rabbit aorta with the selective α1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 ± 4 fmole/106 cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in α1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P

Mark Lyte - One of the best experts on this subject based on the ideXlab platform.

  • Catecholamine inotrope resuscitation of antibiotic damaged staphylococci and its blockade by specific Receptor antagonists
    The Journal of Infectious Diseases, 2008
    Co-Authors: Primrose P E Freestone, Richard D Haigh, Mark Lyte
    Abstract:

    The increasing use of antibiotic-coated catheters, such as those containing rifampin or minocycline, has led to a decrease in catheter colonization by staphylococci but not to a decrease in the incidence of catheter-related bloodstream infection (BSI). Because catheters are used for the administration of Catecholamine inotropes to maintain cardiac function, we examined whether 2 commonly employed inotropes, dopamine and norepinephrine, could affect bacterial viability after exposure to rifampin and minocycline. Rifampin inhibition and minocycline inhibition of staphylococcal growth could be reversed by exposure to dopamine or norepinephrine as a result, in part, of Catecholamine-mediated increased provision of host-sequestered iron. The simultaneous addition of inotropes with an antibiotic did not affect antibiotic susceptibility. Inotrope-induced growth in bacteria previously exposed to antibiotics was blocked by the inclusion in culture media of specific Catecholamine-Receptor antagonists. Considered collectively, these results provide a mechanistic basis for understanding how host-related factors, such as inotrope-based therapeutics, may influence the recovery of antibiotic-stressed bacteria in clinical settings.

  • Blockade of Catecholamine-induced growth by adrenergic and dopaminergic Receptor antagonists in Escherichia coli O157:H7, Salmonella enterica and Yersinia enterocolitica
    BMC Microbiology, 2007
    Co-Authors: Primrose P E Freestone, Richard D Haigh, Mark Lyte
    Abstract:

    Background The ability of Catecholamines to stimulate bacterial growth was first demonstrated just over a decade ago. Little is still known however, concerning the nature of the putative bacterial adrenergic and/or dopaminergic Receptor(s) to which Catecholamines (norepinephrine, epinephrine and dopamine) may bind and exert their effects, or even whether the binding properties of such a Receptor are similar between different species. Results Use of specific Catecholamine Receptor antagonists revealed that only α, and not β, adrenergic antagonists were capable of blocking norepinephrine and epinephrine-induced growth, while antagonism of dopamine-mediated growth was achieved with the use of a dopaminergic antagonist. Both adrenergic and dopaminergic antagonists were highly specific in their mechanism of action, which did not involve blockade of Catecholamine-facilitated iron-acquisition. Use of radiolabeled norepinephrine suggested that the adrenergic antagonists could be acting by inhibiting Catecholamine uptake. Conclusion The present data demonstrates that the ability of a specific pathogen to respond to a particular hormone is dependent upon the host anatomical region in which the pathogen causes disease as well as the neuroanatomical specificity to which production of the particular hormone is restricted; and that both are anatomically coincidental to each other. As such, the present report suggests that pathogens with a high degree of exclusivity to the gastrointestinal tract have evolved response systems to neuroendocrine hormones such as norepinephrine and dopamine, but not epinephrine, which are found with the enteric nervous system.

  • blockade of Catecholamine induced growth by adrenergic and dopaminergic Receptor antagonists in escherichia coli o157 h7 salmonella enterica and yersinia enterocolitica
    BMC Microbiology, 2007
    Co-Authors: Primrose P E Freestone, Richard D Haigh, Mark Lyte
    Abstract:

    The ability of Catecholamines to stimulate bacterial growth was first demonstrated just over a decade ago. Little is still known however, concerning the nature of the putative bacterial adrenergic and/or dopaminergic Receptor(s) to which Catecholamines (norepinephrine, epinephrine and dopamine) may bind and exert their effects, or even whether the binding properties of such a Receptor are similar between different species. Use of specific Catecholamine Receptor antagonists revealed that only α, and not β, adrenergic antagonists were capable of blocking norepinephrine and epinephrine-induced growth, while antagonism of dopamine-mediated growth was achieved with the use of a dopaminergic antagonist. Both adrenergic and dopaminergic antagonists were highly specific in their mechanism of action, which did not involve blockade of Catecholamine-facilitated iron-acquisition. Use of radiolabeled norepinephrine suggested that the adrenergic antagonists could be acting by inhibiting Catecholamine uptake. The present data demonstrates that the ability of a specific pathogen to respond to a particular hormone is dependent upon the host anatomical region in which the pathogen causes disease as well as the neuroanatomical specificity to which production of the particular hormone is restricted; and that both are anatomically coincidental to each other. As such, the present report suggests that pathogens with a high degree of exclusivity to the gastrointestinal tract have evolved response systems to neuroendocrine hormones such as norepinephrine and dopamine, but not epinephrine, which are found with the enteric nervous system.

Susanna Cotecchia - One of the best experts on this subject based on the ideXlab platform.

  • Antagonism of Catecholamine Receptor Signaling by Expression of Cytoplasmic Domains of the Receptors
    Science (New York N.Y.), 1993
    Co-Authors: Louis M. Luttrell, Susanna Cotecchia, Jacek Ostrowski, Humphrey E. Kendall, Robert J. Lefkowitz
    Abstract:

    The actions of many hormones and neurotransmitters are mediated by the members of a superfamily of Receptors coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins). These Receptors are characterized by a highly conserved topographical arrangement in which seven transmembrane domains are connected by intracellular and extracellular loops. The interaction between these Receptors and G proteins is mediated in large part by the third intracellular loop of the Receptor. Coexpression of the third intracellular loop of the alpha 1B-adrenergic Receptor with its parent Receptor inhibited Receptor-mediated activation of phospholipase C. The inhibition extended to the closely related alpha 1C-adrenergic Receptor subtype, but not the phospholipase C-coupled M1 muscarinic acetylcholine Receptor nor the adenylate cyclase-coupled D1A dopamine Receptor. These results suggest that the Receptor-G protein interface may represent a target for Receptor antagonist drugs.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. The authors have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and they now report a possible mechanism for this. Binding studies in rabbit aorta with the selective alpha 1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 {plus minus} 4 fmole/10(6) cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in alpha 1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P less than 0.05). This increased affinity for norepinephrine was associated with a greater increase in 32P-labeled phosphatidylinositol (148% intimal thickening versus 76% control) and phosphatidic acid (151% intimal thickening versus 56% control) following norepinephrine stimulation of free floating rings of intimal hyperplastic aorta. These data suggest that the Catecholamine supersensitivity in rabbit aortic intimal hyperplasia is Receptor mediated and may be linked to the phosphatidylinositol cycle.

  • Altered Catecholamine Receptor affinity in rabbit aortic intimal hyperplasia.
    Journal of Surgical Research, 1991
    Co-Authors: O'malley Mk, Susanna Cotecchia, Per-otto Hagen
    Abstract:

    Abstract Intimal thickening is a universal response to endothelial denudation and is also thought to be a precursor of atherosclerosis. We have demonstrated selective supersensitivity in arterial intimal hyperplasia to norepinephrine and we now report a possible mechanism for this. Binding studies in rabbit aorta with the selective α1-adrenergic radioligand 125I-HEAT demonstrated that there was no change in Receptor density (20 ± 4 fmole/106 cells) in intact vascular smooth muscle cells at either 5 or 14 days after denudation. However, competition studies showed a 2.6-fold increase in α1-adrenergic Receptor affinity for norepinephrine in intimal hyperplastic tissue (P