Role of α-Adrenergic Receptors in the Effect of the β-Adrenergic Receptor Ligands, CGP 12177, Bupranolol, and SR 59230A, on the Contraction of Rat Intrapulmonary Artery

2004 ◽  
Vol 309 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Véronique Leblais ◽  
Fabrice Pourageaud ◽  
M. Dolores Ivorra ◽  
Christelle Guibert ◽  
Roger Marthan ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Ligands ◽  
Cgp 12177 ◽  
Adrenergic Receptor Ligands

scholarly journals Role of beta-adrenergic receptor subtypes in pig uterus contractility with inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Domestic Animals ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptor ◽  
Pharmacological Modulation ◽  
Uterine Inflammation ◽  
Myometrial Contractility

AbstractUterine inflammation is a very common and serious condition in domestic animals. To development and progression of this pathology often lead disturbances in myometrial contractility. Participation of β1-, β2- and β3-adrenergic receptors (ARs) in noradrenaline (NA)-influenced contractility of the pig inflamed uterus was studied. The gilts of SAL- and E.coli-treated groups were administered saline or E.coli suspension into the uterine horns, respectively. Laparotomy was only done in the CON group. Compared to the period before NA administration, this neurotransmitter reduced the tension, amplitude and frequency in uterine strips of the CON and SAL groups. In the E.coli group, NA decreased the amplitude and frequency, and these parameters were lower than in other groups. In the CON, SAL and E.coli groups, β1- and β3-ARs antagonists in more cases did not significantly change and partly eliminated NA inhibitory effect on amplitude and frequency, as compared to NA action alone. In turn, β2-ARs antagonist completely abolished NA relaxatory effect on these parameters in three groups. Summarizing, NA decreases the contractile amplitude and frequency of pig inflamed uterus via all β-ARs subtypes, however, β2-ARs have the greatest importance. Given this, pharmacological modulation of particular β-ARs subtypes can be used to increase inflamed uterus contractility.

scholarly journals Structure-based discovery of  2-adrenergic receptor ligands

2009 ◽  
Vol 106 (16) ◽  
pp. 6843-6848 ◽  
Author(s):  
P. Kolb ◽  
D. M. Rosenbaum ◽  
J. J. Irwin ◽  
J. J. Fung ◽  
B. K. Kobilka ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Ligands ◽  
Adrenergic Receptor Ligands

scholarly journals Diverse arrestin-recruiting and endocytic profiles of tricyclic antipsychotics acting as direct α 2A adrenergic receptor ligands

2017 ◽  
Vol 116 ◽  
pp. 38-49 ◽  
Author(s):  
Christopher Cottingham ◽  
Pulin Che ◽  
Wei Zhang ◽  
Hongxia Wang ◽  
Raymond X. Wang ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Ligands ◽  
Adrenergic Receptor Ligands

1-Arylpiperazinyl-4-cyclohexylamine derived isoindole-1,3-diones as potent and selective α-1a/1d adrenergic receptor ligands

2007 ◽  
Vol 17 (6) ◽  
pp. 1646-1650 ◽  
Author(s):  
Shengjian Li ◽  
George Chiu ◽  
Virginia L. Pulito ◽  
Jingchun Liu ◽  
Peter J. Connolly ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Ligands ◽  
Adrenergic Receptor Ligands

scholarly journals Noradrenergic control of central oxytocin release during lactation in rats

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Additional Experiment ◽  
Adrenergic Agonist ◽  
Magnocellular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Oxytocin Release ◽  
Stimulation Of

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.

scholarly journals Heat and α1-adrenergic responsiveness in human skeletal muscle feed arteries: the role of nitric oxide

2012 ◽  
Vol 113 (11) ◽  
pp. 1690-1698 ◽  
Author(s):  
Stephen J. Ives ◽  
Robert H. I. Andtbacka ◽  
Sun Hyung Kwon ◽  
Yan-Ting Shiu ◽  
Ting Ruan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Human Skeletal Muscle ◽  
Bovine Endothelial Cells ◽  
No Bioavailability ◽  
Feed Arteries ◽  
Skeletal Muscle Feed Arteries

Increased local temperature exerts a sympatholytic effect on human skeletal muscle feed arteries. We hypothesized that this attenuated α1-adrenergic receptor responsiveness may be due to a temperature-induced increase in nitric oxide (NO) bioavailability, thereby reducing the impact of the α1-adrenergic receptor agonist phenylephrine (PE). Thirteen human skeletal muscle feed arteries were harvested, and wire myography was used to generate PE concentration-response curves at 37°C and 39°C, with and without the NO synthase (NOS) inhibitor NG-monomethyl-l-arginine (l-NMMA). A subset of arteries ( n = 4) were exposed to 37°C or 39°C, and the protein content of endothelial NOS (eNOS) and α1-adrenergic receptors was determined by Western blot analysis. Additionally, cultured bovine endothelial cells were exposed to static or shear stress conditions at 37°C and 39°C and assayed for eNOS activation (phosphorylation at Ser1177), eNOS expression, and NO metabolites [nitrate + nitrite (NOx)]. Maximal PE-induced vasocontraction (PEmax) was lower at 39°C than at 37°C [39 ± 10 vs. 84 ± 30% maximal response to 100 mM KCl (KClmax)]. NO blockade restored vasocontraction at 39°C to that achieved at 37°C (80 ± 26% KClmax). Western blot analysis of the feed arteries revealed that heating increased eNOS protein, but not α1-adrenergic receptors. Heating of bovine endothelial cells resulted in greater shear stress-induced eNOS activation and NOx production. Together, these data reveal for the first time that, in human skeletal muscle feed arteries, NO blockade can restore the heat-attenuated α1-adrenergic receptor-mediated vasocontraction and implicate endothelium-derived NO bioavailability as a major contributor to heat-induced sympatholysis. Consequently, these findings highlight the important role of vasodilators in modulating the vascular response to vasoconstrictors.

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