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Journal articles on the topic 'Adenosine A1 antagonist'

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Published: 4 June 2021

Last updated: 5 February 2022

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1

Jackson, Edwin K., Dongmei Cheng, Stevan P. Tofovic, and Zaichuan Mi. "Endogenous adenosine contributes to renal sympathetic neurotransmission via postjunctional A1 receptor-mediated coincident signaling." American Journal of Physiology-Renal Physiology 302, no. 4 (2012): F466—F476. http://dx.doi.org/10.1152/ajprenal.00495.2011.

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Adenosine A1 receptor antagonists have diuretic/natriuretic activity and may be useful for treating sodium-retaining diseases, many of which are associated with increased renal sympathetic tone. Therefore, it is important to determine whether A1 receptor antagonists alter renal sympathetic neurotransmission. In isolated, perfused rat kidneys, renal vasoconstriction induced by renal sympathetic nerve simulation was attenuated by 1) 1,3-dipropyl-8-p-sulfophenylxanthine (xanthine analog that is a nonselective adenosine receptor antagonist, but is cell membrane impermeable and thus does not block

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2

Lee, H. Thomas, and Charles W. Emala. "Protective effects of renal ischemic preconditioning and adenosine pretreatment: role of A1 and A3receptors." American Journal of Physiology-Renal Physiology 278, no. 3 (2000): F380—F387. http://dx.doi.org/10.1152/ajprenal.2000.278.3.f380.

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Renal ischemia and reperfusion during aortic and renal transplant surgery result in ischemic-reperfusion injury. Ischemic preconditioning and adenosine infusion before ischemia protect against ischemic-reperfusion injury in cardiac and skeletal muscle, but these protective phenomena have not been demonstrated in the kidney. Rats were randomized to sham operation, 45-min renal ischemia, ischemic preconditioning with four cycles of 8-min renal ischemia and 5-min reperfusion followed by 45-min renal ischemia, systemic adenosine pretreatment before 45-min renal ischemia, or pretreatments with sele

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3

Carlström, Mattias, Christopher S. Wilcox, and William J. Welch. "Adenosine A2 receptors modulate tubuloglomerular feedback." American Journal of Physiology-Renal Physiology 299, no. 2 (2010): F412—F417. http://dx.doi.org/10.1152/ajprenal.00211.2010.

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Adenosine can mediate the tubuloglomerular (TGF) response via activation of A1 receptors on the afferent arteriole, but both adenosine A1 and A2 receptors can regulate preglomerular resistance. We tested the hypothesis that adenosine A2 receptors offset the effect of A1 receptors and modulate the TGF. Maximal TGF responses were measured in male Sprague-Dawley rats as changes in proximal stop-flow pressure (ΔPSF) in response to increased perfusion of the loop of Henle (0 to 40 nl/min) with artificial tubular fluid (ATF). The maximal TGF response was studied after 5 min of intratubular perfusion

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4

Mozaffari, Mahmood S., Worku Abebe, and Brett K. Warren. "Renal adenosine A3 receptors in the rat: assessment of functional role." Canadian Journal of Physiology and Pharmacology 78, no. 5 (2000): 428–32. http://dx.doi.org/10.1139/y00-007.

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The functional roles of adenosine A3 receptors in the rat kidney were assessed for the first time with respect to A1 receptor-mediated responses. Utilizing a chronically instrumented conscious rat preparation, we tested renal excretory responses to acute administration of the A3 receptor antagonists 3-ethyl - 5-benzyl-2-methyl-6-phenyl- 4-phenylethynyl-1,4-(+)-dihydropridine-3,5-dicarboxylate (MRS-1191) and 9-chloro-2-(2-furyl)-5-phenylacetylamino- [1,2,4]-triazolo[1,5-c]quinazoline (MRS-1220) with reference to the effects of the A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX

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5

Auchampach, J. A., and G. J. Gross. "Adenosine A1 receptors, KATP channels, and ischemic preconditioning in dogs." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (1993): H1327—H1336. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1327.

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The objective of the present study was to characterize the role of adenosine in myocardial ischemic preconditioning in the canine heart. Preconditioning with 5 min of ischemia resulted in a marked reduction in infarct size after 60 min of left circumflex coronary artery occlusion and 5 h of reperfusion in barbital-anesthetized dogs compared with dogs that were not preconditioned (4.8 +/- 1.9 vs. 27.9 +/- 4.5%; P < 0.05). Pretreatment with either the nonselective adenosine receptor antagonist PD 115199 or the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine block

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6

Olivera, A., M. Tomas, and J. M. Lopez-Novoa. "Effect of adenosine A1 and A2 agonists and antagonists on cAMP and Ca2+ in cultured rat mesangial cells." American Journal of Physiology-Cell Physiology 262, no. 4 (1992): C840—C844. http://dx.doi.org/10.1152/ajpcell.1992.262.4.c840.

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Rat glomeruli have been shown to exhibit A1 and A2 adenosine (ADO) receptors. Adenosine also contracts isolated glomeruli and cultured mesangial cells (MC). We studied the effect of the relatively selective ADO agonists R-N6-(1-methyl-1-phenylethyl)adenosine (R-PIA; A1) and 5'-(N-ethylcarboxamido)-adenosine (NECA; A2) on adenosine 3',5'-cyclic monophosphate (cAMP) levels and 45Ca influx in MC. R-PIA (10(-6) M) induced a 55% decrease in cAMP content in 5 microM forskolin-pretreated MC. NECA (10(-6) M) significantly increases by 68% the cAMP levels of forskolin-stimulated MC. NECA-included incre

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7

van Rensburg, HelenaDorathea Janse, LesetjaJ Legoabe, Gisella Terre’Blanche, and MiethaM Van der Walt. "2–Benzylidene–1–Indanone Analogues as Dual Adenosine A1/A2a Receptor Antagonists for the Potential Treatment of Neurological Conditions." Drug Research 69, no. 07 (2019): 382–91. http://dx.doi.org/10.1055/a-0808-3993.

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AbstractPrevious studies explored 2-benzylidine-1-tetralone derivatives as innovative adenosine A1 and A2A receptor antagonists for alternative non-dopaminergic treatment of Parkinson’s disease. This study’s aim is to investigate structurally related 2-benzylidene-1-indanones with substitutions on ring A and B as novel, potent and selective adenosine A1 and A2A receptor blockers. 2-Benzylidene-1-indanone derivatives were synthesised via acid catalysed aldol condensation reactions and evaluated via radioligand binding assays to ascertain structure activity relationships to govern A1 and A2A AR

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8

Coulson, R., P. S. Proch, R. A. Olsson, C. E. Chalfant, and D. R. Cooper. "Upregulated renal adenosine A1 receptors augment PKC and glucose transport but inhibit proliferation." American Journal of Physiology-Renal Physiology 270, no. 2 (1996): F263—F274. http://dx.doi.org/10.1152/ajprenal.1996.270.2.f263.

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Adenosine A1 receptor densities were increased in cultured LLC-PK1 and OK cells by chronic treatment with the adenosine receptor antagonists 1,3,7-trimethylxanthine (caffeine, 1 mM) and 1,3-dimethyl-8-cyclopentylxanthine [cyclopentyltheophylline (CPT), < or = 0.4 mM], respectively. The A1 receptor number per cell was increased twofold by 10-day treatments with 1 mM caffeine or 0.1 mM CPT, and the sodium-coupled glucose uptake was augmented twofold by 1 mM caffeine and sevenfold by 0.1 microM CPT (higher doses of CPT were progressively less stimulatory). Glucose uptake was blocked by acute (

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9

Montandon, Gaspard, Richard Kinkead, and Aida Bairam. "Disruption of adenosinergic modulation of ventilation at rest and during hypercapnia by neonatal caffeine in young rats: role of adenosine A1 and A2A receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 4 (2007): R1621—R1631. http://dx.doi.org/10.1152/ajpregu.00514.2006.

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Caffeine is commonly used to treat respiratory instabilities related to prematurity. However, the role of adenosinergic modulation and the potential long-term effects of neonatal caffeine treatment (NCT) on respiratory control are poorly understood. To address these shortcomings, we tested the following hypotheses: 1) adenosine A1- and A2A-receptor antagonists modulate respiratory activity at rest and during hypercapnia; 2) NCT has long-term consequences on adenosinergic modulation of respiratory control. Rat pups received by gavage either caffeine (15 mg/kg) or water (control) once a day from

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10

Norton, Gavin R., Angela J. Woodiwiss, Robert J. McGinn, et al. "Adenosine A1receptor-mediated antiadrenergic effects are modulated by A2a receptor activation in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 2 (1999): H341—H349. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h341.

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Presently, the physiological significance of myocardial adenosine A2a receptor stimulation is unclear. In this study, the influence of adenosine A2a receptor activation on A1 receptor-mediated antiadrenergic actions was studied using constant-flow perfused rat hearts and isolated rat ventricular myocytes. In isolated perfused hearts, the selective A2a receptor antagonists 8-(3-chlorostyryl)caffeine (CSC) and 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM-241385) potentiated adenosine-mediated decreases in isoproterenol (Iso; 10−8 M)-elicited contractil

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11

Schepp, W., A. H. Soll, and J. H. Walsh. "Dual modulation by adenosine of gastrin release from canine G-cells in primary culture." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 4 (1990): G556—G563. http://dx.doi.org/10.1152/ajpgi.1990.259.4.g556.

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The effects of adenosine on gastrin release were studied in enzymatically dispersed canine antral cells after 24-36 h in primary culture. We found two contrasting actions for adenosine: inhibition of forskolin-stimulated gastrin release and potentiation of bombesin-stimulated gastrin release. These actions appeared to be mediated by A1 and A2 receptors, respectively. Forskolin-stimulated gastrin release was reduced by adenosine and the A1-selective agonist N6-(L-2-phenylisopropyl)adenosine (L-PIA) but not by the A2-selective agonist 2-phenylaminoadenosine (CV 1808). This inhibition by adenosin

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12

Pérez-Pinzón, Miguel A., Peter L. Lutz, Thomas J. Sick, and Myron Rosenthal. "Adenosine, a “Retaliatory” Metabolite, Promotes Anoxia Tolerance in Turtle Brain." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (1993): 728–32. http://dx.doi.org/10.1038/jcbfm.1993.93.

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Contrary to what is found in most vertebrates, the brains of certain turtle species maintain ATP levels and ion homeostasis and survive prolonged anoxia. The hypothesis tested here is that the release of adenosine and its binding to A1 receptors are essential for this anoxic tolerance. Studies were conducted in the isolated turtle cerebellum, which did release adenosine to the extracellular space during anoxia. When adenosine receptor antagonists [theophylline, 8-cyclopentyltheophylline (CPT), or 8-cyclopentyl-1,3-dipropylxanthine (DPCPX)] were added to the superfusate under control conditions

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13

Imai, E., M. Fujii, Y. Kohno, et al. "Adenosine A1 receptor antagonist improves intradialytic hypotension." Kidney International 69, no. 5 (2006): 877–83. http://dx.doi.org/10.1038/sj.ki.5000088.

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14

Huang, M. H., C. Sylven, M. Horackova, and J. A. Armour. "Ventricular sensory neurons in canine dorsal root ganglia: effects of adenosine and substance P." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 2 (1995): R318—R324. http://dx.doi.org/10.1152/ajpregu.1995.269.2.r318.

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Effects elicited by adenosine and substance P on ventricular sensory endings of 14 dorsal root ganglion afferent neurons were studied in situ in anesthetized dogs. Sensory-field application of adenosine (1 microM) increased the activity of these neurons by 179%. Application of a nonspecific adenosine antagonist to epicardial sensory fields suppressed ongoing activity in all 14 neurons by 39%. Application of an A1- or A2-adenosine-receptor antagonist suppressed activity generated by 10 of these neurons by 44 and 59%, respectively. Adenosine applied after A1- or A2-receptor blockade increased ac

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15

Khimenko, P. L., T. M. Moore, L. W. Hill, et al. "Adenosine A2 receptors reverse ischemia-reperfusion lung injury independent of beta-receptors." Journal of Applied Physiology 78, no. 3 (1995): 990–96. http://dx.doi.org/10.1152/jappl.1995.78.3.990.

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To evaluate the adenosine systems ability to reverse the endothelial damage produced by ischemia and reperfusion (I/R), we studied several different selective adenosine-receptor agonists and antagonists, a protein kinase A inhibitor, and a beta-adrenoreceptor antagonist in isolated buffer-perfused rat lungs. I/R (45 min/105 min) produced a sixfold increase in endothelial permeability as measured by the capillary filtration coefficient. Both a selective A2-receptor agonist (CGS-21680, 300 nM) and a beta-receptor agonist (isoproterenol, 10 microM) reversed the increased microvascular permeabilit

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16

Fan, Ming, Weixi Qin, and S. Jamal Mustafa. "Characterization of adenosine receptor(s) involved in adenosine-induced bronchoconstriction in an allergic mouse model." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 6 (2003): L1012—L1019. http://dx.doi.org/10.1152/ajplung.00353.2002.

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We recently reported that adenosine caused bronchoconstriction and enhanced airway inflammation in an allergic mouse model. In this study, we further report the characterization of the subtype of adenosine receptor(s) involved in bronchoconstriction. 5′-( N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist, elicited bronchoconstriction in a dose-dependent manner. Little effects of N 6-cyclopentyladenosine (A1-selective agonist) and 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamidoadenosine (A2A-selective agonist) compared with NECA were observed in this model. 2-Chlo

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17

Li, Xinhui, and James C. Eisenach. "Adenosine Reduces Glutamate Release in Rat Spinal Synaptosomes." Anesthesiology 103, no. 5 (2005): 1060–65. http://dx.doi.org/10.1097/00000542-200511000-00021.

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Background A1 adenosine receptor activation reduces hypersensitivity in animal models of chronic pain, but intrathecal adenosine does not produce analgesia to acute noxious stimuli. Here, the authors test whether increased inhibition by adenosine of glutamate release from afferents after injury accounts for this difference. Methods Synaptosomes were prepared from the dorsal half of the lumbar spinal cord of normal rats or those with spinal nerve ligation. Glutamate release evoked by the TRPV-1 receptor agonist, capsaicin, was measured. Adenosine with or without adenosine A1 and A2 receptor ant

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18

Bozarov, Andrey, Yu-Zhong Wang, Jun Ge Yu, et al. "Activation of adenosine low-affinity A3 receptors inhibits the enteric short interplexus neural circuit triggered by histamine." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 6 (2009): G1147—G1162. http://dx.doi.org/10.1152/ajpgi.00295.2009.

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We tested the novel hypothesis that endogenous adenosine (eADO) activates low-affinity A3 receptors in a model of neurogenic diarrhea in the guinea pig colon. Dimaprit activation of H2 receptors was used to trigger a cyclic coordinated response of contraction and Cl− secretion. Contraction-relaxation was monitored by sonomicrometry (via intracrystal distance) simultaneously with short-circuit current ( Isc, Cl− secretion). The short interplexus reflex coordinated response was attenuated or abolished by antagonists at H2 (cimetidine), 5-hydroxytryptamine 4 receptor (RS39604), neurokinin-1 recep

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19

Macala, Lawrence J., and John P. Hayslett. "Basolateral and apical A1 adenosine receptors mediate sodium transport in cultured renal epithelial (A6) cells." American Journal of Physiology-Renal Physiology 283, no. 6 (2002): F1216—F1225. http://dx.doi.org/10.1152/ajprenal.00085.2002.

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There are conflicting reports in the literature regarding the adenosine receptor that mediates the increase in sodium transport in the A6 cell. In this study we used specific A1 and A2 adenosine receptor agonists and antagonists, as well as two different subclones of the A6 cell, to determine which adenosine receptor mediates the increase in sodium transport. In the A6S2 subclone, basolateral and apical N 6-cyclohexyladenosine (CHA), a selective A1 receptor agonist, stimulated sodium transport at a threshold concentration <10−7 M, whereas CGS-21680, a selective A2 receptor agonist, had a th

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Lasley, Robert D., Gentian Kristo, Byron J. Keith, and Robert M. Mentzer. "The A2a/A2b receptor antagonist ZM-241385 blocks the cardioprotective effect of adenosine agonist pretreatment in in vivo rat myocardium." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (2007): H426—H431. http://dx.doi.org/10.1152/ajpheart.00675.2006.

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There is increasing evidence for interactions among adenosine receptor subtypes in the brain and heart. The purpose of this study was to determine whether the adenosine A2a receptor modulates the infarct size-reducing effect of preischemic administration of adenosine receptor agonists in intact rat myocardium. Adult male rats were submitted to in vivo regional myocardial ischemia (25 min) and 2 h reperfusion. Vehicle-treated rats were compared with rats pretreated with the A1 agonist 2-chloro- N6-cyclopentyladenosine (CCPA, 10 μg/kg), the nonselective agonist 5′- N-ethylcarboxamidoadenosine (N

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21

Tung, Avery, Stacy Herrera, Martin J. Szafran, Kristen Kasza, and Wallace B. Mendelson. "Effect of Sleep Deprivation on Righting Reflex in the Rat Is Partially Reversed by Administration of Adenosine A1 and A2 Receptor Antagonists." Anesthesiology 102, no. 6 (2005): 1158–64. http://dx.doi.org/10.1097/00000542-200506000-00015.

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Background Similarities between naturally occurring sleep and general anesthesia suggest that the two states may interact physiologically. The authors have previously demonstrated that sleep deprivation potentiates anesthetic-induced loss of righting reflex (LORR) in rats. One possible mediator for this effect is adenosine, which accumulates in the brains of sleep-deprived animals and reduces anesthetic requirements. The authors tested in rats the hypothesis that potentiating effects of sleep deprivation on LORR can be altered by adenosine A1 and A2a receptor antagonists. Methods Five experime

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Suleiman, J., and M. Ashraf. "Adenosine attenuates calcium paradox injury: role of adenosine A1 receptor." American Journal of Physiology-Cell Physiology 268, no. 4 (1995): C838—C845. http://dx.doi.org/10.1152/ajpcell.1995.268.4.c838.

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The present study was conducted to test the hypothesis that adenosine attenuates the Ca2+ paradox (PD) injury via stimulation of adenosine A1 receptors linked to Gi proteins in the isolated rat heart. Treatment of adenosine reduced maximum lactate dehydrogenase release and ATP loss compared with regular Ca2+ PD. Recovery of mechanical activity after Ca2+ repletion was observed only in heart treated with adenosine before and during the Ca2+ PD. Significant preservation of myocytes was observed in adenosine-treated hearts compared with the regular Ca2+ PD. Adenosine exerted its effects in a dose

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23

Brager, Darrin H., and Scott M. Thompson. "Activity-Dependent Release of Adenosine Contributes to Short-Term Depression at CA3-CA1 Synapses in Rat Hippocampus." Journal of Neurophysiology 89, no. 1 (2003): 22–26. http://dx.doi.org/10.1152/jn.00554.2002.

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High-frequency stimulation results in a transient, presynaptically mediated decrease in synaptic efficacy called short-term depression (STD). Stimulation of Schaffer-collateral axons at 10 Hz for 5 s resulted in approximately 75% depression of excitatory postsynaptic current (EPSC) slope recorded from CA1 cells in rat organotypic slice cultures. An adenosine A1 receptor antagonist decreased the magnitude of STD elicited with 10-Hz stimulation by approximately 30%. The A1 receptor antagonist had no effect on STD elicited with 3-Hz stimulation. The activation of A1 receptors during 10-Hz stimula

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24

Conlon, Patrick R., and William F. Kiesman. "Synthesis of specifically deuterated adenosine A1 antagonist: BG9928." Journal of Labelled Compounds and Radiopharmaceuticals 50, no. 4 (2007): 219–23. http://dx.doi.org/10.1002/jlcr.1237.

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Terai, Takao, Yasuhiro Kita, Takahiro Kusunoki, et al. "A novel non-xanthine adenosine A1 receptor antagonist." European Journal of Pharmacology 279, no. 2-3 (1995): 217–25. http://dx.doi.org/10.1016/0014-2999(95)00165-h.

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26

Dennis, D., K. Jacobson, and L. Belardinelli. "Evidence of spare A1-adenosine receptors in guinea pig atrioventricular node." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 3 (1992): H661—H671. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h661.

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In normoxic, isolated perfused guinea pig hearts instrumented for measurement of atrioventricular nodal conduction time (AVCT), an analysis utilizing the irreversible A1-adenosine (Ado) antagonist, meta-1,3-phenylene diisothiocyanate xanthine amine cogener (m-DITC-XAC), a novel isothiocyanate derivative of 1,3-dialkylxanthine, was used to investigate whether spare A1-Ado receptors exist in the guinea pig atrioventricular (AV) node and the degree of amplification (reserve) between A1-Ado receptor occupancy and dromotropic response (e.g., AVCT slowing). The potency, dose dependency, and kinetic

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Cano, C., Z. Qureshi, S. Carter, and K. U. Malik. "Contribution of adenosine to isoproterenol-stimulated prostacyclin production in rabbit heart." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 1 (1992): H218—H225. http://dx.doi.org/10.1152/ajpheart.1992.263.1.h218.

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This study investigated adenosine's contribution to isoproterenol-stimulated prostacyclin production, measured as 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) output, and mechanical function in the isolated rabbit heart perfused with Krebs-Henseleit buffer. The isoproterenol-induced increase in 6-keto-PGF1 alpha was diminished by adenosine (10 microM), the A1 receptor antagonist 1,3-dipropyl, 8-cyclopentylxanthine (DPCPX 0.06 microM), and the A2 receptor agonist CGS-21680 (0.6 microM); CGS-21680 did not decrease heart rate (HR) or myocardial contractility (dP/dt(max)). The isoproterenol-in

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Bivalacqua, Trinity J., Hunter C. Champion, David G. Lambert, and Philip J. Kadowitz. "Vasodilator responses to adenosine and hyperemia are mediated by A1 and A2 receptors in the cat vascular bed." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 6 (2002): R1696—R1709. http://dx.doi.org/10.1152/ajpregu.00394.2001.

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Hemodynamic responses to adenosine, the A1 receptor agonists N 6-cyclopentyladenosine (CPA) and adenosine amine congener (ADAC), and the A2 receptor agonist 5′-( N-cyclopropyl)-carboxamido-adenosine (CPCA) were investigated in the hindquarter vascular bed of the cat under constant-flow conditions. Injections of adenosine, CPA, ADAC, CPCA, ATP, and adenosine 5′- O-(3-thiotriphosphate) (ATPγS) into the perfusion circuit induced dose-related decreases in perfusion pressure. Vasodilator responses to the A1 agonists were reduced by the A1 receptor antagonists KW-3902 and CGS-15943, whereas response

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Takeda, M., K. Yoshitomi, and M. Imai. "Regulation of Na(+)-3HCO3- cotransport in rabbit proximal convoluted tubule via adenosine A1 receptor." American Journal of Physiology-Renal Physiology 265, no. 4 (1993): F511—F519. http://dx.doi.org/10.1152/ajprenal.1993.265.4.f511.

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We investigated the role of adenosine A1-receptor in the regulation of basolateral Na(+)-3HCO3- cotransporter in the rabbit proximal convoluted tubule (PCT) microperfused in vitro by monitoring basolateral membrane potential and intracellular pH. FK-453, a highly specific A1 antagonist, inhibited basolateral HCO3- conductance in a concentration-dependent manner (10(-10)-10(-5) M). Other A1 antagonists, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) at 10(-5) M and theophylline at 10(-3) M, also had similar effects. N6-cyclohexyladenosine (CHA) at 10(-7) M attenuated the effect of low concentration

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Stambaugh, K., K. A. Jacobson, J. L. Jiang, and B. T. Liang. "A novel cardioprotective function of adenosine A1 and A3 receptors during prolonged simulated ischemia." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (1997): H501—H505. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h501.

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The possible cardioprotective roles of adenosine A1 and A3 receptors were investigated in a cardiac myocyte model of injury. The adenosine A3 receptor is a novel cardiac receptor capable of mediating potentially important cardioprotective functions. Prolonged hypoxia with glucose deprivation was used to simulate ischemia and to induce injury in cardiac ventricular myocytes cultured from chick embryos 14 days in ovo. When present during the prolonged hypoxia, the adenosine A3 agonists N6-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA) and 2-chloro-N6-(3-iodobenzyl)adenosine-5'-N-methylur

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Teng, Bunyan, Daniel N. Darlington, and Andrew P. Cap. "Adenosine Receptor Identification for Controlling Platelet Aggregation." Blood 132, Supplement 1 (2018): 3733. http://dx.doi.org/10.1182/blood-2018-99-116213.

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Abstract Introduction: Adenosine, an autacoid and metabolite of ATP, has been known to have anti-platelet properties. Of the 4 adenosine receptors, both A2A and/or A2B have been implicated in adenosine-mediated anti-platelet properties, while the roles of A1 and A3 have not been clearly defined in humans. In addition, previous studies show that A2A/A2B on platelets are G-Protein Coupled Receptors and are coupled to a stimulatory G-protein that activate adenylyl cyclase and subsequently increase intracellular cAMP. An elevation of cAMP in platelets inhibits aggregation. In this study, we set ou

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Bauman, L. A., C. D. Mahle, C. G. Boissard, and V. K. Gribkoff. "Age-dependence of effects of A1 adenosine receptor antagonism in rat hippocampal slices." Journal of Neurophysiology 68, no. 2 (1992): 629–38. http://dx.doi.org/10.1152/jn.1992.68.2.629.

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1. Population excitatory postsynaptic potentials (EPSPs) and population spikes evoked in area CA1 of hippocampal slices from aged Fischer 344 rats were significantly smaller in amplitude than responses obtained in slices from young Fischer 344 rats. 2. The A1 adenosine receptor antagonist 8-cyclopentyltheophylline (8-CPT) produced a concentration-dependent increase in synaptic potentials in slices from both young and aged rats. Low concentrations (1 nM) of 8-CPT were effective in producing increases in both population spike amplitudes and population EPSP slopes in young and aged rat slices. Re

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Yasuda, Sally Usdin, Satoru Nagashima, Erwin Douyon, Robert E. Benton, Raymond L. Woosley, and Jean T. Barbey. "Adenosine A1-receptor occupancy predicts A1-receptor antagonist effects of N-0861*." Clinical Pharmacology & Therapeutics 64, no. 5 (1998): 536–41. http://dx.doi.org/10.1016/s0009-9236(98)90136-9.

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Falcón, Jack, Karen Privat, and Jean-Paul Ravault. "Binding of an adenosine A1 receptor agonist and adenosine A1 receptor antagonist to sheep pineal membranes." European Journal of Pharmacology 337, no. 2-3 (1997): 325–31. http://dx.doi.org/10.1016/s0014-2999(97)01305-8.

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Hleihel, W., A. Lafoux, N. Ouaini, and C. Huchet-Cadiou. "Adenosine reduces the reverse mode of the Na+/Ca2+ exchanger in ferret cardiac fibres." Canadian Journal of Physiology and Pharmacology 86, no. 1-2 (2008): 46–54. http://dx.doi.org/10.1139/y07-115.

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The aim of this study was to investigate the effects of adenosine on reverse mode Na+/Ca2+ exchange. In intact ferret cardiac trabeculae, Na+-free contractures were investigated after treating preparations with ryanodine, a sarcoplasmic reticulum Ca2+-channel inhibitor, and thapsigargin, a sarcoplasmic reticulum Ca2+-pump inhibitor added to suppress the sarcoplasmic reticulum function. The effects of adenosine (50–100 nmol/L), adenosine deaminase (ADA, 0.1–0.5 U/L), the A1 and A2A receptor agonists CCPA (3–100 nmol/L) and CGS 21680 (25–100 nmol/L), and the A1 and A2A receptor antagonists DPCPX

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Pan, Sheng-Jun, and Li-Rong Li. "Adenosine A2 receptors are involved in the activation of ATP-sensitive K+ currents during metabolic inhibition in guinea pig ventricular myocytes." Canadian Journal of Physiology and Pharmacology 89, no. 3 (2011): 187–96. http://dx.doi.org/10.1139/y11-010.

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It has been hypothesized that an interaction among adenosine A1 receptors, protein kinase C (PKC) activation, and ATP-sensitive potassium channels (KATP) mediates ischemic preconditioning in experiments on different animal species. The purpose of this study was to determine if activation of KATP is functionally coupled to A1 receptors and (or) PKC activation during metabolic inhibition (MI) in guinea pig ventricular myocytes. Perforated-patch using nystatin and conventional whole-cell recording methods were used to observe the effects of adenosine and adenosine-receptor antagonists on the acti

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Sundin, L., and G. E. Nilsson. "Branchial and systemic roles of adenosine receptors in rainbow trout: an in vivo microscopy study." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 3 (1996): R661—R669. http://dx.doi.org/10.1152/ajpregu.1996.271.3.r661.

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The purinergic branchial vasomotor control in rainbow trout (Oncorhynchus mykiss) was studied using an epi-illumination microscope equipped with a water-immersion objective. Cardiac output (Q), heart rate, and dorsal (PDA) and ventral (PVA) aortic pressures were recorded simultaneously. Prebranchial injection of adenosine or the A1-receptor agonist N6-cyclopentyl-adenosine (CPA) constricted the distal portion of the filament vasculature, which coincided with an increase of PVA. The A2-receptor agonist PD-125944 was without effect. After adenosine and CPA injection, an overflow of blood to the

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Adkins, W. K., J. W. Barnard, T. M. Moore, R. C. Allison, V. R. Prasad, and A. E. Taylor. "Adenosine prevents PMA-induced lung injury via an A2 receptor mechanism." Journal of Applied Physiology 74, no. 3 (1993): 982–88. http://dx.doi.org/10.1152/jappl.1993.74.3.982.

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Previous studies indicate that adenosine attenuates phorbol myristate acetate-(PMA) induced canine lung injury, but the mechanism has not been explained. To evaluate adenosine's protective mechanism, isolated and blood-perfused dog lungs were challenged by PMA (50 micrograms) under control conditions and after both pre- and post-treatment with adenosine and pretreatment with 2-chloro-N6-cyclopentyladenosine (CCPA), 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamido adenosine (CGS 21680C), 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; PD-116948), or isoproterenol. Injury was assessed by me

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Spielman, W. S., K. N. Klotz, L. J. Arend, B. A. Olson, D. G. LeVier, and U. Schwabe. "Characterization of adenosine A1 receptor in a cell line (28A) derived from rabbit collecting tubule." American Journal of Physiology-Cell Physiology 263, no. 2 (1992): C502—C508. http://dx.doi.org/10.1152/ajpcell.1992.263.2.c502.

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We have previously reported that in several renal cell types, adenosine receptor agonists inhibit adenylyl cyclase and activate phospholipase C via a pertussis toxin-sensitive G protein. In the present study, in 28A cells, both of these adenosine receptor-mediated responses were inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a highly selective A1 adenosine receptor antagonist. The binding characteristics of the adenosine A1 receptor in the 28A renal cell line were studied using the radiolabeled antagonist [3H]DPCPX to determine whether two separate binding sites could account for the

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Nagy, L. E., and S. E. F. DeSilva. "Adenosine A1 receptors mediate chronic ethanol-induced increases in receptor-stimulated cyclic AMP in cultured hepatocytes." Biochemical Journal 304, no. 1 (1994): 205–10. http://dx.doi.org/10.1042/bj3040205.

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Cellular responses to adenosine depend on the distribution of the two adenosine receptor subclasses. In primary cultures of rat hepatocytes, adenosine receptors were coupled to adenylate cyclase via A1 and A2 receptors which inhibit and stimulate cyclic AMP production respectively. R-(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA), the adenosine A1 receptor-selective agonist, inhibited glucagon-stimulated cyclic AMP production with an IC50 of 19 nM. This inhibition was blocked by the A1-specific antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPDX). 5′-N- Ethylcarboxamidoadenosine (NECA), an agoni

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Hoenderop, Joost G. J., Anita Hartog, Peter H. G. M. Willems, and René J. M. Bindels. "Adenosine-stimulated Ca2+reabsorption is mediated by apical A1 receptors in rabbit cortical collecting system." American Journal of Physiology-Renal Physiology 274, no. 4 (1998): F736—F743. http://dx.doi.org/10.1152/ajprenal.1998.274.4.f736.

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Confluent monolayers of immunodissected rabbit connecting tubule and cortical collecting duct cells, cultured on permeable supports, were used to study the effect of adenosine on net apical-to-basolateral Ca2+ transport. Apical, but not basolateral, adenosine increased this transport dose dependently from 48 ± 3 to 110 ± 4 nmol ⋅ h−1 ⋅ cm−2. Although a concomitant increase in cAMP formation suggested the involvement of an A2 receptor, the A2 agonist CGS-21680 did not stimulate Ca2+ transport, while readily increasing cAMP. By contrast, the A1 agonist N 6-cyclopentyladenosine (CPA) maximally st

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Pelleg, Amir, and Carl M. Hurt. "Effects of N6-endonorbornan-2-yl-9-methyladenine, N0861, on negative chronotropic and vasodilatory actions of adenosine in the canine heart in vivo." Canadian Journal of Physiology and Pharmacology 70, no. 11 (1992): 1450–56. http://dx.doi.org/10.1139/y92-205.

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The pharmacology of N6-endonorbornan-2-yl-9-methyladenine (N0861), a new selective antagonist of adenosine at the A1 adenosine receptor subtype (A1-AdoR), was studied in vivo using a canine model. First, the pharmacokinetics of N0861 were determined in anesthetized dogs. The time-dependent decay of plasma levels of N0861 fitted a two-compartment polyexponential model with α-phase t1/2 = 3.80 min and β-phase t1/2 = 80.55 min. Secondly, the effect of N0861 on the negative chronotropic and vasodilatory actions of adenosine in the canine heart were determined. N0861 attenuated the negative chronot

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Kusiuioki, T., T. Terai, A. Akahane, et al. "FK352: A NOVEL. WATER-SOLUBLE. A1-SELECTIVE. ADENOSINE ANTAGONIST." Japanese Journal of Pharmacology 67 (1995): 318. http://dx.doi.org/10.1016/s0021-5198(19)47235-1.

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Haleen, S. J., R. P. Steffen, and H. W. Hamilton. "PD 116,948, a highly selective A1 adenosine receptor antagonist." Life Sciences 40, no. 6 (1987): 555–61. http://dx.doi.org/10.1016/0024-3205(87)90369-9.

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Romano, F. D., T. S. Naimi, and J. G. Dobson. "Adenosine attenuation of catecholamine-enhanced contractility of rat heart in vivo." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (1991): H1635—H1639. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1635.

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The antiadrenergic action of adenosine was examined in open- and closed-chest preparations of anesthetized rats. The positive inotropic effects of a jugular vein infusion of either isoproterenol or epinephrine were attenuated by phenylisopropyladenosine, an adenosine A1-receptor agonist. 1,3-Dipropyl,8-cyclopentylxanthine, a specific A1-receptor antagonist, inhibited the action of phenylisopropyladenosine. The results indicate that adenosine receptor-mediated mechanisms are functional in the blood-perfused rodent heart and support the possibility of a physiological role for adenosine in modula

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Stella, Salvatore L., Eric J. Bryson, Lucia Cadetti, and Wallace B. Thoreson. "Endogenous Adenosine Reduces Glutamatergic Output From Rods Through Activation of A2-Like Adenosine Receptors." Journal of Neurophysiology 90, no. 1 (2003): 165–74. http://dx.doi.org/10.1152/jn.00671.2002.

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Adenosine is released from retina in darkness; photoreceptors possess A2 adenosine receptors, and A2 agonists inhibit L-type Ca2+ currents ( ICa) in rods. We therefore investigated whether A2 agonists inhibit rod inputs into second-order neurons and whether selective antagonists to A1, A2A, or A3 receptors prevent Ca2+ influx through rod ICa. [Ca2+]i changes in rods were assessed with fura-2. ICa in rods and light responses of rods and second-order neurons were recorded using perforated patch-clamp techniques in the aquatic tiger salamander retinal slice preparation. Consistent with earlier re

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Mudumbi, R. V., S. C. Montamat, R. F. Bruns, and R. E. Vestal. "Cardiac functional responses to adenosine by PD 81,723, an allosteric enhancer of the adenosine A1 receptor." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 3 (1993): H1017—H1022. http://dx.doi.org/10.1152/ajpheart.1993.264.3.h1017.

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Adenosine, a locally released and rapidly metabolized nucleoside, protects the heart from damage during ischemia by reducing oxygen demand and increasing oxygen supply. The aminothiophene derivative (2-amino-4,5-dimethylthien-3-yl)[3-(trifluoromethyl)phenyl]-met hanone (PD 81,723) has been shown to act as an allosteric enhancer of the adenosine A1 receptor in brain membranes and thyroid cells. The present study investigates the effects of PD 81,723 in spontaneously contracting right atria and electrically stimulated left atria isolated from Sprague-Dawley rats. N6-cyclopentyladenosine (CPA), a

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Freissmuth, M., E. Selzer, and W. Schütz. "Interactions of purified bovine brain A1-adenosine receptors with G-proteins. Reciprocal modulation of agonist and antagonist binding." Biochemical Journal 275, no. 3 (1991): 651–56. http://dx.doi.org/10.1042/bj2750651.

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The bovine brain A1-adenosine receptor was purified 8000-fold by affinity chromatography on xanthine-amine-congener (XAC)-Sepharose. Addition of a 120-fold molar excess of a purified bovine brain G-protein preparation (Go,i a mixture of Go and Gi, containing predominantly Go) decreases the Bmax of the binding of the antagonist radioligand [3H]XAC to the receptor. This decrease is observed not only after insertion into phospholipid vesicles but also in detergent solution, and is reversed by GTP analogues. In the presence of Go,i, about 20 and 40% of the receptors display guanine-nucleotide-sens

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Meno, Joseph R., Alison V. Crum, and H. Richard Winn. "Effect of adenosine receptor blockade on pial arteriolar dilation during sciatic nerve stimulation." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 5 (2001): H2018—H2027. http://dx.doi.org/10.1152/ajpheart.2001.281.5.h2018.

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In the present study, we report the effects of adenosine receptor antagonists on pial vasodilatation during contralateral sciatic nerve stimulation (SNS). The pial circulation was observed through a closed cranial window in α-chloralose-anesthetized rats. In artificial cerebrospinal fluid (CSF), SNS resulted in a 30.5 ± 13.2% increase in pial arteriolar diameter in the hindlimb somatosensory cortex. Systemic administration of the selective adenosine A2A receptor antagonist, 4-(2-{7-amino-2-[2-furyl][3,2,4]triazolol[2,3-a][1,3,5]triazin-5-yl-amino} ethyl)phenol (ZM-241385), significantly ( P &l

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Hanouz, Jean-Luc, Alexandra Yvon, Massimo Massetti, et al. "Mechanisms of Desflurane-induced Preconditioning in Isolated Human Right Atria In Vitro." Anesthesiology 97, no. 1 (2002): 33–41. http://dx.doi.org/10.1097/00000542-200207000-00006.

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Background The authors examined the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, adenosine A1 receptor, and alpha and beta adrenoceptors in desflurane-induced preconditioning in human myocardium, in vitro. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in oxygenated Tyrode's solution (34 degrees C; stimulation frequency, 1 Hz). Before a 30-min anoxic period, 3, 6, and 9% desflurane was administered during 15 min. Desflurane, 6%, was also administered in the presence of 10 microm glibenclamide, a K(ATP) channels antagonist;

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