Strips of human right atrial appendages were preincubated with [3H]noradrenaline and then superfused with physiological salt solution containing inhibitors of uptake1 and uptake2. Tritium overflow was evoked by transmural electrical stimulation (standard frequency: 2 Hz). Prostaglandin E2 (PGE2) inhibited the electrically evoked tritium overflow; at the highest concentration investigated, tritium overflow was reduced by about 80% and the pIC50% value was 7.14. The effect of PGE2 was not affected by rauwolscine, which, by itself, increased the evoked overflow. Naproxen failed to affect the evoked tritium overflow and its inhibition by PGE2. The inhibitory effect of PGE2 on the electrically evoked tritium overflow was mimicked by prostaglandin E1, the EP1/EP3-receptor agonist sulprostone and the EP2/EP3-receptor agonist misoprostol with the rank order of potency (pEC50%): sulprostone (7.68) > misoprostol (7.10) > PGE1 (6.39). In contrast, PGF2alpha, the IP/EP1-receptor agonist iloprost and the stable thromboxane A2 analogue U46619 (9,11-dideoxy-11alpha,9alpha-epoxy-methanoprostaglandin++ + F2alpha) did not change evoked tritium overflow. PGD2 caused facilitation. These results suggest that the sympathetic nerve fibres innervating human atrial appendages are endowed with presynaptic inhibitory EP3 and facilitatory DP-receptors. The EP3-receptors appear not to be tonically activated and do not interact with the alpha2-autoreceptors.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/pl00005276 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Antibodies Against the NH-Terminus of the GluA Subunits Affect the AMPA-Evoked Releasing Activity: The Role of Complement.
Front Immunol
July 2021
Pharmacology and Toxicology Section, Department of Pharmacy, DIFAR, Genoa, Italy.
Article Synopsis
- Antibodies targeting the amino-terminal domain of receptor subunits influence transmitter release efficiency in isolated nerve endings, supporting their presence and suggesting their composition.
- Western blot and confocal microscopy identified the presence of GluA1 to GluA4 receptor subunits in cortical synaptosomes, confirming the existence of AMPA autoreceptors that regulate presynaptic release.
- Modified synaptosomes, treated with specific antibodies, showed increased densities of GluA2 and GluA3 and enhanced AMPA-induced glutamate release, indicating a potential role for these antibodies in altering synaptic activity.
Immuno-Pharmacological Characterization of Presynaptic GluN3A-Containing NMDA Autoreceptors: Relevance to Anti-NMDA Receptor Autoimmune Diseases.
Mol Neurobiol
September 2019
Department of Pharmacy, DiFAR, Pharmacology and Toxicology Section, University of Genoa, Viale Cembrano 4, 16148, Genoa, Italy.
Mouse hippocampal glutamatergic nerve endings express presynaptic release-regulating NMDA autoreceptors (NMDARs). The presence of GluN1, GluN2A, GluN2B, and GluN3A subunits in hippocampal vesicular glutamate transporter type 1-positive synaptosomes was confirmed with confocal microscopy. GluN2C, GluN2D, and GluN3B immunopositivity was scarcely present.
View Article and Find Full Text PDFN-Ethylmaleimide differentiates between the M- and M-autoreceptor-mediated inhibition of acetylcholine release in the mouse brain.
Naunyn Schmiedebergs Arch Pharmacol
November 2018
Institute of Pharmacology and Toxicology, University of Bonn, Sigmund-Freud-Str. 25, 53127 Bonn, Germany.
Article Synopsis
- Muscarinic M and M receptors show similarities in their brain distribution and signaling but differ in G protein coupling, with the M receptor having a more significant coupling to G proteins.
- Research on murine hippocampal and striatal slices indicated that the muscarinic agonist iperoxo inhibits acetylcholine release in both regions but was more effective in the hippocampus compared to the striatum.
- The study suggests that in the striatum, higher concentrations of muscarinic agonists may activate a stimulatory G protein, contrasting with the hippocampus where such activity appears to be less significant.
Direct and Systemic Administration of a CNS-Permeant Tamoxifen Analog Reduces Amphetamine-Induced Dopamine Release and Reinforcing Effects.
Neuropsychopharmacology
September 2017
Department of Pharmacology, University of Michigan, Ann Arbor, MI, USA.
Amphetamines (AMPHs) are globally abused. With no effective treatment for AMPH addiction to date, there is urgent need for the identification of druggable targets that mediate the reinforcing action of this stimulant class. AMPH-stimulated dopamine efflux is modulated by protein kinase C (PKC) activation.
View Article and Find Full Text PDFA search for presynaptic inhibitory histamine receptors in guinea-pig tissues: Further H3 receptors but no evidence for H4 receptors.
Neuropharmacology
July 2016
Institut für Pharmakologie und Toxikologie, Universität Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. Electronic address:
The histamine H4 receptor is coupled to Gi/o proteins and expressed on inflammatory cells and lymphoid tissues; it was suggested that this receptor also occurs in the brain or on peripheral neurones. Since many Gi/o protein-coupled receptors, including the H3 receptor, serve as presynaptic inhibitory receptors, we studied whether the sympathetic neurones supplying four peripheral tissues and the cholinergic neurones in the hippocampus from the guinea-pig are equipped with release-modulating H4 and H3 receptors. For this purpose, we preincubated tissue pieces from the aorta, atrium, renal cortex and vas deferens with (3)H-noradrenaline and hippocampal slices with (3)H-choline and determined the electrically evoked tritium overflow.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!