After one week treatment with caffeine (20 mg/kg i.p.) the number of adenosine receptors, as determined by specific binding of (3H)-L-PIA, in rat cerebral cortical membranes was increased by about 25%. Cyclic AMP accumulation induced by adenosine analogues in slices of rat hippocampus was unaffected by caffeine treatment. The inhibition of lipolysis in rat fat cells by 2-chloro-adenosine was similarly unaffected. The potency of caffeine as an antagonist of these adenosine-receptor mediated effects was not altered by caffeine treatment. It is concluded that at least some adenosine receptors are up-regulated as a consequence of prolonged caffeine treatment, but that the increase in receptor number is not related to changes in at least two effects of adenosine and caffeine.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1748-1716.1982.tb07078.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Role of A adenosine receptor in cardiovascular diseases: Bridging molecular mechanisms with therapeutic opportunities.
Exp Mol Pathol
January 2025
Department of Pharmaceutical Care, Faculty of Pharmacy, Chiang Mai University, Chiang Mai 50200, Thailand. Electronic address:
Adenosine serves as a critical homeostatic regulator, exerting influence over physiological and pathological conditions in the cardiovascular system. During cellular stress, increased extracellular adenosine levels have been implicated in conferring cardioprotective effects through the activation of adenosine receptors with the A adenosine receptor subtype showing the highest expression in the heart. A adenosine receptor stimulation inhibits adenylyl cyclase activity via heterotrimeric G proteins, leading to the activation of distinct downstream effectors involved in cardiovascular homeostasis.
View Article and Find Full Text PDFMCU-i4, a mitochondrial Ca uniporter modulator, induces breast cancer BT474 cell death by enhancing glycolysis, ATP production and reactive oxygen species (ROS) burst.
Oncol Res
January 2025
Department of Physiology, China Medical University, Taichung, 404328, Taiwan.
Objectives: Mitochondrial Ca uniporter (MCU) provides a Ca influx pathway from the cytosol into the mitochondrial matrix and a moderate mitochondrial Ca rise stimulates ATP production and cell growth. MCU is highly expressed in various cancer cells including breast cancer cells, thereby increasing the capacity of mitochondrial Ca uptake, ATP production, and cancer cell proliferation. The objective of this study was to examine MCU inhibition as an anti-cancer mechanism.
View Article and Find Full Text PDFAttributes novel drug candidate: Constitutive GPCR signal bias mediated by purinergic receptors.
Pharmacol Ther
January 2025
School of Pharmacy, China Pharmaceutical University, Nanjing 211198, China; School of Life Science and Technology, China Pharmaceutical University, Nanjing 211198, China.
G protein-coupled receptors (GPCRs) can transmit signals via G protein-dependent or independent pathways due to the conformational changes of receptors and ligands, which is called biased signaling. This concept posits that ligands can selectively activate a specific signaling pathway after receptor activation, facilitating downstream signaling along a preferred pathway. Biased agonism enables the development of ligands that prioritize therapeutic signaling pathways while mitigating on-target undesired effects.
View Article and Find Full Text PDFNew physiological insights using multi-TE ASL MRI measuring blood-brain barrier water exchange after caffeine intake.
MAGMA
January 2025
Imaging Physics, Fraunhofer Institute for Digital Medicine MEVIS, Max-von-Laue-Straße 2, 28359, Bremen, Germany.
Objectives: Caffeine, a known neurostimulant and adenosine antagonist, affects brain physiology by decreasing cerebral blood flow. It interacts with adenosine receptors to induce vasoconstriction, potentially disrupting brain homeostasis. However, the impact of caffeine on blood-brain barrier (BBB) permeability to water remains underexplored.
View Article and Find Full Text PDFThe Anti-Human P2X7 Monoclonal Antibody (Clone L4) Can Mediate Complement-Dependent Cytotoxicity of Human Leukocytes.
Eur J Immunol
January 2025
Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, Australia.
P2X7 is an extracellular adenosine 5'-triphosphate (ATP)-gated cation channel that plays various roles in inflammation and immunity. P2X7 is present on peripheral blood monocytes, dendritic cells (DCs), and innate and adaptive lymphocytes. The anti-human P2X7 monoclonal antibody (mAb; clone L4), used for immunolabelling P2X7 or blocking P2X7 activity, is a murine IgG2 antibody, but its ability to mediate complement-dependent cytotoxicity (CDC) is unknown.
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!