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Artykuły w czasopismach na temat „Adenosine”

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Data publikacji: 4 czerwca 2021

Data aktualizacji: 1 kwietnia 2023

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1

Dibner-Dunlap, M. E., T. Kinugawa i M. D. Thames. "Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues". American Journal of Physiology-Heart and Circulatory Physiology 265, nr 1 (1.07.1993): H395—H400. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h395.

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Adenosine is released during myocardial ischemia and can cause angina-like chest pain when given by intracoronary administration. We tested the hypothesis that intracoronary adenosine activates cardiac sympathetic afferent fibers and results in reflex sympathoexcitation. In dogs with sinoaortic denervation and vagotomy, we administered 2 mg of adenosine into the left anterior descending artery over 2 min. Before dipyridamole infusion, intracoronary adenosine resulted in no change in blood pressure or renal sympathetic nerve activity. After dipyridamole infusion, which blocks adenosine uptake, intracoronary adenosine resulted in a peak increase in sympathetic activity of 34 +/- 7%. We also investigated the adenosine-receptor subtype responsible for this sympathoexcitatory response. We found that the adenosine1 agonist N6-cyclopentyladenosine elicited a dose-dependent sympathoexcitatory response similar to adenosine but that the adenosine2 agonist 5'-(N-cyclopropyl)carboxamidoadenosine failed to elicit a sympathoexcitatory response. We conclude that adenosine activates cardiac sympathetic afferent fibers and leads to a sympathoexcitatory response due to activation of adenosine1 receptors.

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2

Sundin, Emma M., John D. Ciubuc, Kevin E. Bennet, Katia Ochoa i Felicia S. Manciu. "Comparative Computational and Experimental Detection of Adenosine Using Ultrasensitive Surface-Enhanced Raman Spectroscopy". Sensors 18, nr 8 (16.08.2018): 2696. http://dx.doi.org/10.3390/s18082696.

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To better understand detection and monitoring of the important neurotransmitter adenosine at physiological levels, this study combines quantum chemical density functional modeling and ultrasensitive surface-enhanced Raman spectroscopic (SERS) measurements. Combined simulation results and experimental data for an analyte concentration of about 10−11 molar indicate the presence of all known molecular forms resulting from adenosine’s complex redox-reaction. Detailed analysis presented here, besides assessing potential Raman signatures of these adenosinic forms, also sheds light on the analytic redox process and voltammetric detection. Examples of adenosine Raman fingerprints for different molecular orientations with respect to the SERS substrate are the vibrational line around 920 ± 10 cm−1 for analyte physisorption through the carbinol moiety and around 1600 ± 20 cm−1 for its fully oxidized form. However, both hydroxyl/oxygen sites and NH2/nitrogen sites contribute to molecule’s interaction with the SERS environment. Our results also reveal that contributions of partially oxidized adenosine forms and of the standard form are more likely to be detected with the first recorded voltammetric oxidation peak. The fully oxidized adenosine form contributes mostly to the second peak. Thus, this comparative theoretical–experimental investigation of adenosine’s vibrational signatures provides significant insights for advancing its detection, and for future development of opto-voltammetric biosensors.

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3

Eisenach, James C., Regina Curry i David D. Hood. "Dose Response of Intrathecal Adenosine in Experimental Pain and Allodynia". Anesthesiology 97, nr 4 (1.10.2002): 938–42. http://dx.doi.org/10.1097/00000542-200210000-00028.

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Background Intrathecal adenosine reduces areas of mechanical hypersensitivity and provides analgesia in patients with neuropathic pain. Adenosine also causes side effects, yet its dose response for either efficacy or side effects has not been examined in double blind studies. We studied two doses of intrathecal adenosine in humans with experimental hypersensitivity and the ability of the adenosine receptor antagonist, aminophylline, to reverse adenosine's effects. Methods Following Internal Review Board approval and written informed consent, 35 volunteers were studied. Five volunteers were studied to confirm the stability of a new method of inducing hypersensitivity with capsaicin. The remaining 30 volunteers received, in a randomized, double-blind manner, saline, or adenosine, 0.5 or 2.0 mg, by intrathecal injection 40 min after areas of allodynia and hyperalgesia were established from capsaicin. Two hr later, volunteers were randomized to receive intravenous saline or aminophylline, 5 mg/kg. Results Topical capsaicin with intermittent heating resulted in stable areas of allodynia and hyperalgesia. Intrathecal adenosine, but not saline, reduced areas of allodynia and hyperalgesia from capsaicin, with no differences between doses. Side effects occurred in 1, 2, and 6 volunteers receiving saline, 0.5 mg and 2.0 mg adenosine, respectively. Aminophylline failed to reverse adenosine's effects. Conclusions There is no difference in efficacy to experimental hypersensitivity between the largest approved dose of intrathecal adenosine and a dose 25% this size, but side effects are more common with the larger dose. Failure of aminophylline to reverse adenosine's effects could reflect inadequate concentrations at receptors in the spinal cord after intravenous injection.

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4

Chiari, Astrid I., i James C. Eisenach. "Intrathecal Adenosine". Anesthesiology 90, nr 5 (1.05.1999): 1413–21. http://dx.doi.org/10.1097/00000542-199905000-00026.

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Background Spinal adenosine receptor agonists exert antinociception in animal models of acute and chronic pain, but adenosine itself has not been examined. The authors tested the antinociceptive and antihypersensitivity interactions of intrathecal adenosine and its interactions with intrathecal clonidine and neostigmine in rat models of acute thermal nociception and postoperative hypersensitivity. Methods Rats were prepared with lumbar intrathecal catheters. Responses to acute noxious stimulation were evaluated by latency to paw withdrawal from a radiant heat source focused on the hind paw. Postoperative hypersensitivity was measured after an incision in the rat hind paw by application of von Frey filaments to the heel adjacent to the wound. An isobolographic design was used to distinguish between additive and synergistic drug interactions. Results Spinal administration of clonidine and neostigmine, but not adenosine, produced dose-dependent antinociception to noxious thermal stimulation. Addition of adenosine enhanced the antinociceptive effect of clonidine but not neostigmine. In contrast, each of these three agents alone reversed postoperative hypersensitivity. Pretreatment with the alpha-adrenergic antagonist phentolamine completely reversed adenosine's antihypersensitivity action. Adenosine interacted synergistically with neostigmine and additively with clonidine in reducing postoperative hypersensitivity. Conclusions These data indicate that intrathecal adenosine by itself has no antinociceptive properties to acute noxious thermal stimulation in rats, but enhances clonidine's antinociception. In contrast, intrathecal adenosine is active against postoperative hypersensitivity by an adrenergic mechanism. Different interactions between adenosine, clonidine, and neostigmine in acute nociception and postoperative hypersensitivity models are consistent with altered central processing of sensory information after peripheral injury.

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5

Nair, Vasu, Steven Adah i Seung Ha. "Strategically Functionalized Adenosines: Agonists for Adenosine Receptors". Nucleosides, Nucleotides and Nucleic Acids 14, nr 3 (1.05.1995): 537–39. http://dx.doi.org/10.1080/15257779508012421.

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6

Bantel, Carsten, Xinhui Li i James C. Eisenach. "Intraspinal Adenosine Induces Spinal Cord Norepinephrine Release in Spinal Nerve-ligated Rats but not in Normal or Sham Controls". Anesthesiology 98, nr 6 (1.06.2003): 1461–66. http://dx.doi.org/10.1097/00000542-200306000-00024.

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Background Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity. Methods Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min. Results In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated. Conclusions This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.

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7

Vidal, C. "Adenosine and adenosine receptors". Biochimie 74, nr 6 (czerwiec 1992): 591. http://dx.doi.org/10.1016/0300-9084(92)90165-b.

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8

Steinberg, Thomas H. "Adenosine and Adenosine Receptors". American Journal of Respiratory Cell and Molecular Biology 2, nr 2 (luty 1990): 127–28. http://dx.doi.org/10.1165/ajrcmb/2.2.127.

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9

Fredholm, Bertil. "Adenosine and adenosine receptors". Trends in Pharmacological Sciences 12 (styczeń 1991): 76. http://dx.doi.org/10.1016/0165-6147(91)90503-k.

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10

Shang, Liangcheng, Yaobiao Huang, Xin Xie, Sudan Ye i Chun Chen. "Effect of Adenosine Receptor Antagonists on Adenosine-Pretreated PC12 Cells Exposed to Paraquat". Dose-Response 20, nr 2 (kwiecień 2022): 155932582210934. http://dx.doi.org/10.1177/15593258221093411.

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Previous studies evaluated the adenosine receptor antagonists alone to determine their effects on oxidative stress, but little is known about adenosine’s protective efficacy when oxidative injury occurs in vivo. Adenosine is a crucial signaling molecule recognized by four distinct G-protein-coupled receptors (GPCRs) (i.e., A1R, A2AR, A2BR, and A3R) and protects cells against pathological conditions. The present study was performed to evaluate the role of antagonist modulation in the setting of paraquat toxicity with adenosine pretreatment. First, PC12 cells were exposed to paraquat (850 μM) and adenosine (30 μM) to develop an in vitro model for the antagonist effect assay. Second, we found that the A1R antagonist DPCPX enhanced the viability of paraquat-induced PC12 cells that underwent adenosine pretreatment. Moreover, the A2AR antagonist ZM241385 decreased the viability of paraquat-induced PC12 cells that underwent adenosine pretreatment. Our findings indicate that adenosine protection requires a dual blockade of A1R and activation of A2AR to work at its full potential, and the A2B and A3 adenosine receptor antagonists increased paraquat-induced oxidative damage. This represents a novel pharmacological strategy based on A1/A2A interactions and can assist in clarifying the role played by AR antagonists in the treatment of neurodegenerative diseases.

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11

Makarchikov, A. F., T. V. Saroka i T. G. Kudyrka. "Adenosine thiamine triphosphate and adenosine thiamine triphosphate hydrolase activity in animal tissues". Ukrainian Biochemical Journal 90, nr 4 (22.06.2018): 52–63. http://dx.doi.org/10.15407/ubj90.04.052.

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12

Ling, Chunyan, Liangcheng Shang, Xin Xie, Sudan Ye, Ningjing Wang i Chun Chen. "AdoR-1 (Adenosine Receptor) Contributes to Protection against Paraquat-Induced Oxidative Stress in Caenorhabditis elegans". Oxidative Medicine and Cellular Longevity 2022 (22.12.2022): 1–13. http://dx.doi.org/10.1155/2022/1759009.

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AdoR-1, the single adenosine receptor homolog in Caenorhabditis elegans, which belongs to the superfamily of G-protein coupled receptors (GPCRs), mediates most of the physiological effects of extracellular adenosine. Adenosine has been proved to improve the survival rate of C. elegans in oxidative stress conditions. However, the potential mechanism of adenosine’s protective effect against oxidative stress via AdoR-1 has not been studied. In this study, C. elegans were divided into three groups: two groups with paraquat treatment, one in the presence and one in the absence of adenosine, and an untreated control group. Results indicate that many differentially expressed genes were found to be enriched significantly in neural-related signaling pathways among transcriptome data of three groups. Further gene network analysis showed that some important genes well known to be involved in promoting the acetylcholine release pathway, such as dop-1, egl-30, and unc-13, and those involved in promoting the neuropeptide release pathway, such as kin-1, were upregulated by paraquat induction but downregulated after adenosine treatment. Meanwhile, a completely opposite trend was observed for the goa-1 gene that inhibits the acetylcholine-release and neuropeptide-release pathway. Additionally, some biochemical assays including SOD, GSSG, GSH, and AChE were measured to identify the potential protection of adenosine against oxidative stress between wild-type strain N2 and ador-1 gene knockout strain EG6890. Conclusively, our study revealed series of adenosine receptor-mediated genes in C. elegans that might act as regulators of paraquat-induced oxidative stress and may indicate adenosine’s promising protective effects.

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13

Warner, Eve L., Franco Galasso, Carl I. Thompson i Francis L. Belloni. "Vasodilative and anti-adrenergic effects of adenosine in diabetic rat hearts". Canadian Journal of Physiology and Pharmacology 70, nr 1 (1.01.1992): 13–19. http://dx.doi.org/10.1139/y92-003.

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To determine the vasodilative and negative inotropic effects of adenosine in hearts of diabetic rats, isolated hearts, perfused at constant perfusion pressure (Langendorff technique), were prepared from age-matched control Wistar rats and rats made diabetic 10 weeks prior to study by a single injection of streptozotocin (65 mg∙kg−1, i.p.). Adenosine and nitroprusside each increased coronary inflow when administered either as bolus injections or as infusions. Coronary flow responses to nitroprusside were unchanged in diabetic hearts. Coronary flow responses of diabetic hearts to adenosine injections were unchanged, but responses to adenosine infusions tended to be larger than in normal hearts. Diabetes had no significant effect on the EC50 for either vasodilator. Adenosine inhibited the inotropic effect of isoproterenol (enhanced left ventricular (LV) pressure (P) and LV dP/dtmax) in normal hearts, independently of its vasodilative action. This negative inotropic action of adenosine appeared equally strong in diabetic hearts. We conclude that adenosine's coronary vasodilative and anti-β-adrenergic, negative inotropic effects in the rat heart were not diminished after 10 weeks of streptozotocin-induced diabetes mellitus. Thus, earlier reports of diminished adenosine dilative efficacy in experimental diabetes may have been unique to those particular models.Key words: experimental diabetes mellitus, coronary, adenosine, isoproterenol, myocardial contraction.

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14

Hilleman, Daniel E., B. Daniel Lucas, Syed M. Mohiuddin i M. Jeffrey Holmberg. "Cost-Minimization Analysis of Intravenous Adenosine and Dipyridamole in Thallous Chloride ti 201 Spect Myocardial Perfusion Imaging". Annals of Pharmacotherapy 31, nr 9 (wrzesień 1997): 974–79. http://dx.doi.org/10.1177/106002809703100903.

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Objective To conduct a cost-minimization analysis of intravenous adenosine and intravenous dipyridamole in thallous chloride TI 201 single-photon emission computed tomography (SPECT) myocardial perfusion imaging. Design A retrospective, open-label, cost-minimization analysis. Setting University hospital, outpatient nuclear medicine department. Patients Eighty-three patients undergoing dipyridamole TI 201 SPECT and 166 patients undergoing adenosine TI 201 SPECT. Main outcome Measures A cost-minimization analysis was conducted using a direct cost accounting approach estimating institutional costs. For the purpose of this study, sensitivity and specificity between adenosine SPECT and dipyridamole SPECT were assumed to be identical. Key costs evaluated included acquisition, administration, monitoring, treatment of adverse effects, follow-up care, and repeat tests. Results Adenosine increased heart rate and lowered blood pressure to a significantly greater extent than dipyridamole. The frequency of adverse reactions was not significantly different (p = 0.103) between adenosine (1.64 ± 1.32 per patient) and dipyridamole (1.36 ± 1.23 per patient). The frequency of prolonged and late-onset adverse effects was significantly greater for dipyridamole than for adenosine (p < 0.001). The frequency of adverse events requiring medical intervention was statistically greater for dipyridamole (24%) compared with adenosine (5%) (p < 0.00001). Total cost was significantly less for adenosine ($378.50 ± $128.20 per patient) compared with dipyridamole ($485.60 ± $230.40). Although adenosine had a significantly greater acquisition cost than dipyridamole (p < 0.0001), administration, monitoring, and adverse reaction costs were significantly less for adenosine than for dipyridamole. Conclusions The cost of using dipyridamole is significantly greater than the cost of using adenosine despite adenosine's high acquisition cost. Adenosine is less expensive to use because of lower administration costs, monitoring costs, and adverse effect costs. Adenosine should be the agent of choice for pharmacologic vasodilation in the setting of myocardial perfusion imaging.

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Bullough, D. A., M. J. Magill, G. S. Firestein i K. M. Mullane. "Adenosine activates A2 receptors to inhibit neutrophil adhesion and injury to isolated cardiac myocytes." Journal of Immunology 155, nr 5 (1.09.1995): 2579–86. http://dx.doi.org/10.4049/jimmunol.155.5.2579.

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Abstract Inhibition of neutrophil-myocyte adhesion and adhesion-dependent myocyte injury by adenosine was evaluated using isolated TNF-alpha-activated canine cells. Adenosine inhibited adhesion of activated neutrophils to cardiac myocytes with an IC50 of 11 +/- 4 nM. Inhibition of neutrophil adhesion (92 +/-3% by 100 nM adenosine) led to inhibition of myocyte injury (by 90 +/- 6%, as assessed by dye exclusion). Inhibition of cell adhesion by adenosine was blocked by the A2 antagonist, 1,3-dimethyl-1-propylxanthine, but not by the A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine. Moreover, the A2 agonist, CGS21680 (2-[4-(2-carboxymethyl)phenethylamino]-5'-N-ethylcarboxamido adenosine), but not the A1 agonist, N6-cyclopentyladenosine, mimicked adenosine in preventing cell adhesion. These observations implicate the A2 receptor in the mechanism of inhibition of cell adhesion. pretreatment and washing of neutrophils, but not cardiac myocytes, with adenosine or CGS21680 led to inhibition of adhesion, suggesting that the neutrophil A2 receptor is the target of adenosine's action. In contrast, inhibition of cell adhesion by adenosine was poteniated by 8-cyclopentyl-1,3-dipropylxanthine (IC50 = 4 +/- 1 nM) and attenuated by N6-cyclopentyladenosine, suggesting that occupancy of A1 receptors can conversely increase cell adhesion. Neutrophil-myocyte adhesion was inhibited by acadesine (IC50 = 12 +/- 2 microM) also via an adenosine-dependent mechanism because it was blocked by 1,3-dimethyl-1-propylxanthine or adenosine deaminase, an enzyme that degrades any adenosine that is formed. Acadesine-induced inhibition if cell adhesion (83 +/- 4% by 100 microM) resulted in inhibition of myocyte injury (by 76 +/- 6%). Other adenosine-regulating agents, including the acadesine analogue, GP531 (5-amino-1 beta-D-(5-benzylamino-5-deoxyribofuranosyl) imidazole-4-carboxamide), and inhibitors of adenosine transport and intracellular metabolism also inhibited cell adhesion. These results indicate that exogenous or endogenous adenosine can inhibit neutrophil-myocyte adhesion and injury in cells activated with TNF-alpha by an A2-mediated mechanism. Although the predominant activity of adenosine is to attenuate cell adhesion, stimulation of A1 receptors has the opposite effect, i.e., to augment adhesive interactions.

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16

Li, J., i E. R. Perl. "Adenosine inhibition of synaptic transmission in the substantia gelatinosa". Journal of Neurophysiology 72, nr 4 (1.10.1994): 1611–21. http://dx.doi.org/10.1152/jn.1994.72.4.1611.

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1. We studied adenosine's action on synaptic transmission from primary afferent fibers to neurons of the substantia gelatinosa (SG) using tight-seal whole cell recordings in transverse slices of hamster spinal cord. Adenosine had two actions, hyperpolarization of the postsynaptic membrane and depression of the excitatory postsynaptic currents (EPSCs) evoked by dorsal root stimulation. 2. Under voltage clamp adenosine elicited a sustained outward current at a holding potential of -70 mV. The outward current was blocked by a combination of intracellular cesium and tetraethylammonium, an effect characteristic of potassium channels. The adenosine-induced current reversed at -97 +/- 6 (SD) mV, close to the potassium equilibrium potential. These observations suggest that adenosine activates a potassium conductance in SG neurons so as to inhibit primary afferent synaptic transmission postsynaptically. 3. Adenosine reduced the miniature EPSC frequency without significantly changing the amplitude. In contrast, the glutamate receptor competitive antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) substantially reduced the amplitudes of miniature EPSCs while producing a much smaller effect on the miniature frequency than adenosine. In evoked EPSCs adenosine reduced unitary content without reducing unitary amplitude. The effects on both miniature and evoked EPSCs suggest that adenosine inhibits synaptic currents by suppressing presynaptic transmitter release. 4. EPSCs evoked by dorsal root stimuli were subdivided into monosynaptic and polysynaptic categories. Adenosine at superfusion concentrations of 20-300 microM suppressed all polysynaptic EPSCs. Less than half of monosynaptic EPSCs were inhibited, usually those evoked by the slowest-conducting primary afferents. These observations were interpreted to indicate that a principal action of adenosine in SG is on interneuronal communication.

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17

Zhulai, Galina, Eugenia Oleinik, Mikhail Shibaev i Kirill Ignatev. "Adenosine-Metabolizing Enzymes, Adenosine Kinase and Adenosine Deaminase, in Cancer". Biomolecules 12, nr 3 (8.03.2022): 418. http://dx.doi.org/10.3390/biom12030418.

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The immunosuppressive effect of adenosine in the microenvironment of a tumor is well established. Presently, researchers are developing approaches in immune therapy that target inhibition of adenosine or its signaling such as CD39 or CD73 inhibiting antibodies or adenosine A2A receptor antagonists. However, numerous enzymatic pathways that control ATP-adenosine balance, as well as understudied intracellular adenosine regulation, can prevent successful immunotherapy. This review contains the latest data on two adenosine-lowering enzymes: adenosine kinase (ADK) and adenosine deaminase (ADA). ADK deletes adenosine by its phosphorylation into 5′-adenosine monophosphate. Recent studies have revealed an association between a long nuclear ADK isoform and an increase in global DNA methylation, which explains epigenetic receptor-independent role of adenosine. ADA regulates the level of adenosine by converting it to inosine. The changes in the activity of ADA are detected in patients with various cancer types. The article focuses on the biological significance of these enzymes and their roles in the development of cancer. Perspectives of future studies on these enzymes in therapy for cancer are discussed.

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18

Nascimento, Valter A., Petr Melnikov i Lourdes Z. Z. Consolo. "Computerized Modeling of Adenosine Triphosphate, Adenosine Triarsenate and Adenosine Trivanadate". Molecules 17, nr 8 (8.08.2012): 9489–95. http://dx.doi.org/10.3390/molecules17089489.

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Rouquette, Marie, Sinda Lepetre-Mouelhi, Ophélie Dufrançais, Xue Yang, Julie Mougin, Grégory Pieters, Sébastien Garcia-Argote, Adriaan P. IJzerman i Patrick Couvreur. "Squalene-Adenosine Nanoparticles: Ligands of Adenosine Receptors or Adenosine Prodrug?" Journal of Pharmacology and Experimental Therapeutics 369, nr 1 (22.01.2019): 144–51. http://dx.doi.org/10.1124/jpet.118.254961.

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Heller, L. J., G. J. Trachte i J. F. Regal. "Role of adenosine in hypoxic alterations of anaphylaxis of isolated guinea pig hearts". American Journal of Physiology-Heart and Circulatory Physiology 257, nr 5 (1.11.1989): H1378—H1388. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1378.

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Previous studies suggest that high levels of adenosine may enhance histamine release and contribute to atrioventricular (AV) nodal conduction arrhythmias during anaphylaxis of isolated guinea pig hearts. To determine whether elevations in endogenous adenosine evoked by hypoxic conditions have similar effects, isolated hearts of guinea pigs passively sensitized by intracardiac injection were perfused with solutions equilibrated with 95% O2 (normoxia) or 30% O2 (hypoxia). When compared with normoxia, hypoxia before antigen challenge increased adenosine release, decreased vascular resistance, and prolonged P-R intervals, whereas hypoxia during anaphylaxis potentiated the increase in adenosine release, attenuated the increases in vascular resistance and atrial rate, and increased the occurrence of conduction arrhythmias without altering the antigen-induced release of either histamine or thromboxane. Addition of the adenosine receptor antagonist 8-(4-sulfophenyl)theophylline (SP-T) to the hypoxic perfusate significantly decreased antigen-induced release of histamine and thromboxane. These data indicate that 1) hypoxia-induced depression of antigen-induced mediator release may be counteracted by the stimulatory effect of the increased adenosine induced by hypoxia, and 2) under hypoxic conditions, adenosine's negative dromotropic, chronotropic, and vasodilatory effects may influence the anaphylactic reaction.

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Armstead, W. M. "Role of Nitric Oxide, Cyclic Nucleotides, and the Activation of ATP-Sensitive K+ Channels in the Contribution of Adenosine to Hypoxia-Induced Pial Artery Dilation". Journal of Cerebral Blood Flow & Metabolism 17, nr 1 (styczeń 1997): 100–108. http://dx.doi.org/10.1097/00004647-199701000-00013.

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Previously, it had been observed that nitric oxide (NO) contributes to hypoxia-induced pial artery dilation in the newborn pig. Additionally, it was also noted that activation of ATP-sensitive K+ channels (KATP) contribute to cGMP-mediated as well as to hypoxia-induced pial dilation. Although somewhat controversial, adenosine is also thought to contribute to hypoxic cerebrovasodilation. The present study was designed to investigate the role of NO, cyclic nucleotides, and activation of KATP channels in the elicitation of adenosine's vascular response and relate these mechanisms to the contribution of adenosine to hypoxia-induced pial artery dilation. The closed cranial window technique was used to measure pial diameter in newborn pigs. Hypoxia-induced artery dilation was attenuated during moderate (PaO2 ≈ 35 mm Hg) and severe hypoxia (PaO2 ≈ 25 mm Hg) by the adenosine receptor antagonist 8-phenyltheophylline (8-PT) (10–5 M) (26 ± 2 vs. 19 ± 2 and 34 ± 2 vs. 22 ± 2% for moderate and severe hypoxia in the absence vs. presence of 8-PT, respectively). This concentration of 8-PT blocked pial dilation in response to adenosine (8 ± 2, 16 ± 2, and 23 ± 2 vs. 2 ± 2, 4 ± 2, and 6 ± 2% for 10–8, 10–6, and 10–4 M adenosine before and after 8-PT, respectively). Similar data were also obtained using adenosine deaminase as a probe for the role of adenosine in hypoxic pial dilation. Adenosine-induced dilation was associated with increased CSF cGMP concentration (390 ± 11 and 811 ± 119 fmol/ml for control and 10–4 M adenosine, respectively). The NO synthase inhibitor, L-NNA, and the cGMP antagonist, Rp 8-bromo cGMPs, blunted adenosine-induced pial dilation (8 ± 1, 14 ± 1, and 20 ± 3 vs. 3 ± 1, 5 ± 1, and 8 ± 3% for 10–8, 10–6, and 10–4 M adenosine before and after L-NNA, respectively). Adenosine dilation was also blunted by glibenclamide, a KATP antagonist (9 ± 2, 14 ± 3, 21 ± 4 vs. 4 ± 1, 8 ± 2, and 11 ± 2% for 10–8, 10–6, and 10–4 M adenosine before and after glibenclamide, respectively). Finally, it was also observed that adenosine-induced dilation was associated with increased CSF cAMP concentration and the cAMP antagonist, Rp 8-bromo cAMPs, blunted adenosine pial dilation. These data show that adenosine contributes to hypoxic pial dilation. These data also show that NO, cGMP, cAMP, and activation of KATP channels all contribute to adenosine induced pial dilation. Finally, these data suggest that adenosine contributes to hypoxia-induced pial artery dilation via cAMP and activation of KATP channels by NO and cGMP.

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Carré, David A., Claire H. Mitchell, Kim Peterson-Yantorno, Miguel Coca-Prados i Mortimer M. Civan. "Adenosine stimulates Cl− channels of nonpigmented ciliary epithelial cells". American Journal of Physiology-Cell Physiology 273, nr 4 (1.10.1997): C1354—C1361. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1354.

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Ciliary epithelial cells possess multiple purinergic receptors, and occupancy of A1 and A2 adenosine receptors is associated with opposing effects on intraocular pressure. Aqueous adenosine produced increases in short-circuit current across rabbit ciliary epithelium, blocked by removing Cl− and enhanced by aqueous Ba2+. Adenosine’s actions were further studied with nonpigmented ciliary epithelial (NPE) cells from continuous human HCE and ODM lines and freshly dissected bovine cells. With gramicidin present, adenosine (≥3 μM) triggered isosmotic shrinkage of the human NPE cells, which was inhibited by the Cl− channel blockers 5-nitro-2-(3-phenylpropylamino)benzoate (NPPB) and niflumic acid. At 10 μM, the nonmetabolizable analog 2-chloroadenosine and AMP also produced shrinkage, but not inosine, UTP, or ATP. 2-Chloroadenosine (≥1 μM) triggered increases of whole cell currents in HCE cells, which were partially reversible, Cl− dependent, and reversibly inhibited by NPPB. Adenosine (≥10 μM) also stimulated whole cell currents in bovine NPE cells. We conclude that occupancy of adenosine receptors stimulates Cl− secretion in mammalian NPE cells.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1389 (luty 2012): 7. http://dx.doi.org/10.2165/00128415-201213890-00016.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1396 (kwiecień 2012): 7. http://dx.doi.org/10.2165/00128415-201213960-00020.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 703 (maj 1998): 6. http://dx.doi.org/10.2165/00128415-199807030-00018.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 746 (kwiecień 1999): 6. http://dx.doi.org/10.2165/00128415-199907460-00016.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1161 (lipiec 2007): 6. http://dx.doi.org/10.2165/00128415-200711610-00017.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1190 (luty 2008): 6. http://dx.doi.org/10.2165/00128415-200811900-00019.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1131 (grudzień 2006): 6. http://dx.doi.org/10.2165/00128415-200611310-00008.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1359 (lipiec 2011): 7. http://dx.doi.org/10.2165/00128415-201113590-00018.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 544 (kwiecień 1995): 4. http://dx.doi.org/10.2165/00128415-199505440-00006.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 548 (kwiecień 1995): 4. http://dx.doi.org/10.2165/00128415-199505480-00009.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 445 (kwiecień 1993): 4. http://dx.doi.org/10.2165/00128415-199304450-00007.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 449 (maj 1993): 5. http://dx.doi.org/10.2165/00128415-199304490-00008.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 450 (maj 1993): 5. http://dx.doi.org/10.2165/00128415-199304500-00015.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 460 (lipiec 1993): 5. http://dx.doi.org/10.2165/00128415-199304600-00017.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 463 (sierpień 1993): 5. http://dx.doi.org/10.2165/00128415-199304630-00015.

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Faulds, Diana, Paul Chrisp i Micaela M. T. Buckley. "Adenosine". Drugs 41, nr 4 (kwiecień 1991): 596–624. http://dx.doi.org/10.2165/00003495-199141040-00007.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 610 (lipiec 1996): 7. http://dx.doi.org/10.2165/00128415-199606100-00022.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 800 (maj 2000): 5. http://dx.doi.org/10.2165/00128415-200008000-00009.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1401 (maj 2012): 5. http://dx.doi.org/10.2165/00128415-201214010-00014.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 387 (luty 1992): 4. http://dx.doi.org/10.2165/00128415-199203870-00011.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 395 (kwiecień 1992): 5. http://dx.doi.org/10.2165/00128415-199203950-00012.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 417 (wrzesień 1992): 4. http://dx.doi.org/10.2165/00128415-199204170-00007.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1198 (kwiecień 2008): 5. http://dx.doi.org/10.2165/00128415-200811980-00016.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1221 (wrzesień 2008): 7. http://dx.doi.org/10.2165/00128415-200812210-00017.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1275 (październik 2009): 7. http://dx.doi.org/10.2165/00128415-200912750-00017.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1251 (maj 2009): 4. http://dx.doi.org/10.2165/00128415-200912510-00007.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1257 (czerwiec 2009): 6. http://dx.doi.org/10.2165/00128415-200912570-00015.

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&NA;. "Adenosine". Reactions Weekly &NA;, nr 1301 (maj 2010): 7. http://dx.doi.org/10.2165/00128415-201013010-00023.

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