Phosphorus-31 nuclear magnetic resonance studies of adenosine 5'-triphosphate bound to a nitrated derivative of G-actin
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ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTPhosphorus-31 nuclear magnetic resonance studies of adenosine 5'-triphosphate bound to a nitrated derivative of G-actinManfred Brauer and Brian D. SykesCite this: Biochemistry 1981, 20, 24, 6767–6775Publication Date (Print):November 1, 1981Publication History Published online1 May 2002Published inissue 1 November 1981https://pubs.acs.org/doi/10.1021/bi00527a005https://doi.org/10.1021/bi00527a005research-articleACS PublicationsRequest reuse permissionsArticle Views56Altmetric-Citations23LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-AlertsKeywords:
Derivative (finance)
Adenosine triphosphate
Inosine
Adenosine Deaminase Inhibitor
Adenosine A1 receptor
Deoxycoformycin
Purinergic Signalling
Deamination
Hypoxanthine
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The isolated taenia coli of the guinea pig takes up tritiated adenosine, adenosine monophosphate, adenosine diphosphate, and adenosine triphosphate, in preference to tritiated inosine and adenine. After uptake, [(3)H]adenosine is converted and retained primarily as [(3)H]adenosine triphosphate. Tritium is released from taenia coli treated with [(3)H]adenosine upon activation of the nonadrenergic inhibitory nerves. These results are consistent with the previous evidence that adenosine triphosphate may be the transmitter from the nerves.
Adenosine triphosphate
Taenia coli
Adenosine monophosphate
Inosine
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It has been recognized for many years that the purine nucleoside adenosine exerts numerous effects in mammalian myocardium. During the last decade, an in particular over the last 5 years, substantial evidence has accumulated that adenosine also exerts beneficial effects in the ischemic/reperfused myocardium. The cardioprotective effects of adenosine are manifest by attenuation of reversible postischemic ventricular dysfunction (i.e., stunning) and reduction of myocardial infarct size. These effects can be produced by augmenting endogenous adenosine levels with adenosine deaminase inhibitors and nucleoside transport inhibitors and by infusing adenosine (intracoronary or intravenous). Similar to adenosine's effects in nonischemic hearts, the cardioprotective effects of adenosine are mediated by activation of extracellular adenosine receptors. The results of studies with adenosine receptor agonists and antagonists indicate that adenosine's beneficial effect in reversibly and irreversibly injured myocardium is mediated primarily via adenosine A1 receptor activation. The protective effects of adenosine appear to occur during ischemia since adenosine infusion during reperfusion neither attenuates stunning nor reduces infarct size. Adenosine is cardioprotective in rats, rabbits, dogs, and pigs, and initial clinical reports indicate that adenosine may enhance myocardial protection during open heart surgery in humans. This review will summarize the current state of knowledge on the cardioprotective effects of adenosine in experimental and clinical studies. Drug Dev. Res. 39:314–318, 1996 © 1997 Wiley-Liss, Inc.
Adenosine A3 receptor
Adenosine Deaminase Inhibitor
Adenosine A1 receptor
Purinergic Signalling
Myocardial Stunning
Cardioprotection
Adenosine kinase
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Adenosine triphosphate
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Adenosine test was proposed as a tool for identification of syncopal patients who benefit from pacemaker implantation. Aim of the study was to assess the relationship between adenosine levels, the outcome of adenosine test and results of implantable loop recorder (ILR) monitoring in patients with syncope.In 29 patients (mean age 59 ± 11 years, 15 men, 14 women) with unexplained syncope ILR was implanted. In addition, adenosine test (intravenous injection of 20 mg adenosine bolus) and assays of plasmatic adenosine and adenosine-deaminase were performed.Adenosine test was positive in 15 patients and negative in 14 patients. Patients with positive adenosine test had lower adenosine levels compared to patients with negative test (8.86 ± 2.07 ng/ml vs. 15.18 ± 2.14 ng/ml, p = .04). No difference was observed in adenosine deaminase levels (16.35 ± 2.20 IU/l vs. 13.20 ± 2.48 IU/l, p = .40). There was a negative correlation between adenosine level and AVB duration during adenosine test (p = .04; R2 = 0.22). Patients with positive adenosine test had more frequent asystole during ILR monitoring than patients with negative test (9 pts vs. 1 pt, p = .005). Adenosine levels were lower in patients with asystolic syncope on ILR compared to vasodepressor syncope 8.20 ± 2.86 ng/ml versus 13.27 ± 7.26 ng/ml, p = .05).Patients with positive adenosine test have decreased production of endogenous adenosine compared to patients with negative adenosine test. Positivity of adenosine test and low adenosine level in the peripheral blood were associated with more frequent asystolic episodes during ILR monitoring.
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In these experiments we tested the quantitative importance of adenosine as a mediator in the regulation of muscle with blood containing adenosine at concentrations more than 1,000 times the normal resting adenosine level (1, 7) so that the effect of any endogenously released adenosine would be miniscule in comparison with the effect of this perfused adenosine. Therefore, any major blood flow responses that should occur while the muscle remained continuously under the influence of the perfused adenosine could hardly be ascribed to endogenous adenosine. At the onset of the perfusion with the adenosine the blood flow increased approximately sevenfold. However, over 1-3 h of continued perfusion, the blood flow returned to or near to control despite the extreme amounts of adenosine. Then, while the muscle was still exposed to the adenosine, both reactive hyperemia and exercise hyperemia were elicited for varying time periods and varying degrees for a total of 96 separate measurements in 12 preparations. In all instances the increases in blood flow during hyperemia were almost exactly identical to those recorded prior to adenosine perfusion. Because it would have been almost impossible for the small amounts of endogenous adenosine to cause the large hyperemia responses in the face of the extreme amounts of perfused adenosine, it is concluded that both the reactive and exercise hyperemia responses are probably caused either entirely or almost entirely by factors other than adenosine.
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Cyclic 39, 59-[14C]AMP was measured in platelets that had first been incubated with [14C]adenine. Maximum increases of 2-4-fold were observed 0.5 min after addition of 10-40 µM adenosine. Smaller increases were obtained with higher concentrations of adenosine. In 0.5-min incubations 2-chloroadenosine was less effective than adenosine at concentrations below 20 µM and more effective at concentrations above 100 µM. Incorporation of 1-10 µM adenosine into platelets was inhibited at least 96% by p-nitrobenzylthioguanosine without any effect on the increase in cyclic [14C]AMP caused by these concentrations of adenosine, suggesting that adenosine acts at an extracellular site. With higher adenosine concentrations, p-nitrobenzylthioguanosine was less effective in inhibiting incorporation of adenosine but blocked the decline in cyclic [14C]AMP levels observed on increasing the adenosine concentration above 40 µM. This inhibitory effect of high adenosine concentrations on the accumulation of cyclic [14C]AMP was more easily detected when adenosine was added with prostaglandin E1 and represents a second, possibly intracellular action of adenosine unrelated to its effect in increasing cyclic AMP levels. Papaverine markedly potentiated the increase in platelet cyclic [14C]AMP observed with all concentrations of adenosine, indicating that adenosine activates platelet adenylate cyclase. The kinetics of this activation were studied in intact platelets incubated for short intervals in the presence of papaverine. Adenosine (K A = 1 µM) activated platelet adenylate cyclase up to a maximum of 8-10-fold. This action of adenosine was competitively inhibited by caffeine (Ki = 72 µM) or theophylline (Ki = 25 µM). No inhibitory effect of high adenosine concentrations on cyclic [14C]AMP formation was observed in intact platelets in the presence of papaverine. The plateletaggregating agents ADP and epinephrine, but not vasopressin, markedly inhibited the increase in platelet cyclic [14C]AMP with adenosine. ADP was found to be a noncompetitive inhibitor (Ki = 0.9 µM) of the effect of adenosine on adenylate cyclase in intact platelets. Some close correlations were observed between the effects of adenosine on platelet cyclic [14C]AMP levels and on platelet aggregation. Caffeine partially blocked the inhibition of aggregation by adenosine. As a whole the results show that platelets possess a specific extracellular membrane receptor for adenosine, which is distinct from that for ADP and which mediates the inhibition of platelet function by adenosine by activating platelet adenylate cyclase.
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Adenosine triphosphate
Diphosphoglycerate
Blood preservation
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Abstract: The stereoenantiomers D‐[ 3 H]adenosine and L‐[ 3 H]adenosine were used to study adenosine accumulation in rat cerebral cortical synaptoneurosomes. L‐Adenosine very weakly inhibited rat brain adenosine deaminase (ADA) activity with a K i value of 385 μ M . It did not inhibit rat brain adenosine kinase (AK) activity, nor was it utilized as a substrate for either ADA or AK. The rate constants (fmol/mg of protein/s) for L‐[ 3 H]adenosine accumulation measured in assays where transport was stopped either with inhibitor‐stop centrifugation or with rapid filtration methods were 82 ± 14 and 75 ± 10, respectively. Using the filtration method, the rates of L‐[ 3 H]adenosine accumulation were not significantly different from the value of 105 ± 15 fmol/mg of protein/s measured for D‐[ 3 H]adenosine transport. Unlabeled D‐adenosine and nitrobenzylthioinosine, both at a concentration of 100 μ M , reduced the levels and rates of L‐[ 3 H]adenosine accumulation by >44%. These findings suggest that L‐adenosine, a metabolically stable enantiomeric analog, and the naturally occurring D‐adenosine are both taken up by rat brain synaptoneurosomes by similar processes, and as such L‐adenosine may represent an important new probe with which adenosine uptake may be studied.
Adenosine kinase
Adenosine A1 receptor
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The effect of adenosine and some related compound was studied on blood flow in feline oral mucosa. Changes in the rate of disappearance of 125Iodine (k-value) from a local depot in the oral mucosa was used to determine changes in the mucosal blood flow. Infusion of adenosine caused a dose-dependent increase of blood flow. Two stable adenosine analogues, adenosine 5'- ethylcarboxamide ( NECA ) and L-phenylisopropyl-adenosine (L-PIA), were 20 and 10 times more potent than the parent compound. Dipyridamole (2 mg/kg), which blocks adenosine uptake, significantly enhanced the potency of adenosine. Theophylline (10 mg/kg) inhibited the vasodilatory effect of adenosine and of the adenosine analogues. The result suggest that adenosine may be involved in the regulation of blood flow in the oral mucosa.
Aminophylline
Dipyridamole
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