Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of adenosine deaminase, inosine, alkylxanthines (8-phenyltheophylline (8-PT), theophylline and isobutylmethylxanthine (IBMX], dipyridamole, alpha, beta-methylene ADP (AOPCP) and ATP analogues (alpha, beta-methylene ATP and beta, gamma-methylene ATP) on evoked end-plate potentials (e.p.p.s) were investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with tubocurarine. The effects of 8-PT and IBMX on the amplitude and quantal content of e.p.p.s were also investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with high-magnesium solutions. 2. Adenosine deaminase reversibly increased the amplitude of e.p.p.s and prevented the reduction caused by exogenously applied adenosine on e.p.p. amplitude. The increase caused by adenosine deaminase was equivalent to the decrease caused by 12 +/- 5.8 microM-adenosine on e.p.p. amplitude. 3. Inosine, the product of adenosine deamination, was virtually devoid of effect on e.p.p.s. 4. The adenosine receptor antagonists at the frog neuromuscular junction, 8-PT and theophylline, increased in a concentration-dependent manner the amplitude of e.p.p.s in the presence of tubocurarine. 8-PT increased the amplitude and quantal content of e.p.p.s in the presence of high magnesium. IBMX, which does not behave as an adenosine receptor antagonist at the frog neuromuscular junction, decreased the amplitude of e.p.p.s in the presence of tubocurarine or high-magnesium solutions. 5. Dipyridamole, an adenosine uptake blocker, decreased the amplitude of e.p.p.s, and in a concentration that did not affect neuromuscular transmission potentiated the depressing effect of adenosine, but not that of 2-chloroadenosine, on the amplitude of e.p.p.s. 6. AOPCP, an inhibitor of 5'-nucleotidase, increased the amplitude of e.p.p.s and markedly attenuated the depressing effect of ATP, but not that of adenosine, on e.p.p. amplitude. 7. The ATP analogue, alpha, beta-methylene ATP, which is not a substrate for 5'-nucleotidase, was virtually devoid of effect on e.p.p.s. beta, gamma-Methylene ATP, which can be a substrate for 5'-nucleotidase, mimicked the depressing effect of ATP on e.p.p. amplitude, an effect which was also reduced by AOPCP. 8. It is concluded that in conditions in which the initial quantal content is assumed to be normal (1) endogenous adenosine depresses neuromuscular transmission, (2) at the neuromuscular junction adenosine is inactivated through a dipyridamole-sensitive uptake process, and (3) released adenine nucleotides might contribute to the pool of endogenous adenosine which modulates neuromuscular transmission.
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PMID:On the role, inactivation and origin of endogenous adenosine at the frog neuromuscular junction. 282 Dec 40

The role of adenosine in postcontraction hyperemia (PCH) following sustained, maximal isometric contractions was studied in free-flowing dog gracilis muscles. The hemodynamic responses to contraction were examined in the presence and absence of dipyridamole (an adenosine transport inhibitor), erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA, an adenosine deaminase inhibitor), or alpha, beta-methyleneadenosine-5'-diphosphate (AOPCP, an inhibitor of 5'-nucleotidase). Each muscle was stimulated to contract for 1, 3, 5, and 10 s during saline and drug infusions. For each contraction, the tension-time integral (TT), excess flow (EQ), and excess oxygen consumption (EVo2) were computed. Linear regression analyses were then performed on EQ vs. TT, EVo2 vs. TT, and EQ vs. EVo2. An alteration of the PCH response by the drug was determined as any significant change from the saline control in the slope of the linear regression of EQ vs. EVo2. Dipyridamole and EHNA caused increases of 73 and 48%, respectively, in the slope of EQ vs. EVo2, whereas AOPCP decreased the slope by 41%. The changes in the PCH produced by these drugs are consistent with the hypothesis that an increase in interstitial adenosine during muscular contraction contributes to PCH.
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PMID:Adenosine as a mediator of postcontraction hyperemia in dog gracilis muscle. 669 37

The aim of this study was to determine whether ATP must be hydrolysed to adenosine in order to activate the P1-purinoceptor. Isometric contractions of electrically paced guinea-pig isolated left atria were recorded. Purines evoked negative inotropic responses that were competitively antagonised by theophylline. The order of agonist potency was 2-chloroadenosine greater than adenosine greater than beta, gamma-methylene ATP greater than ATP. Adenosine deaminase alone, or combined with 5'-nucleotidase, attenuated responses to adenosine and 5' AMP, respectively, but did not decrease those to ATP or beta, gamma-methylene ATP. Inhibition of 5'-nucleotidase did not alter responses to ATP. Dipyridamole potentiated responses to ATP both in the absence and in the presence of adenosine deaminase. Alpha, beta-methylene ATP had little agonist activity, however this was not due to its resistance to hydrolysis as the stable beta, gamma-methylene isostere of ATP was a potent agonist. These results indicate that hydrolysis of ATP to adenosine or 5' AMP is not a pre-requisite for activation of the P1-receptor in the guinea-pig atrium.
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PMID:Can ATP stimulate P1-receptors in guinea-pig atrium without conversion to adenosine? 689 58

Although dipyridamole has been extensively studied as an anti-aggregating agent, its mechanism of action has not been elucidated. Cultured mesangial cells were treated with dipyridamole 1-100 microM from 6-72 h. Ecto-5'-nucleotidase activity approximately doubled (from 115 +/- 11 to 226 +/- 14 nmol/min/mg) after treatment with 100 microM dipyridamole for 72 h. This effect was concentration- and time-dependent. Cycloheximide, an inhibitor of protein synthesis, did not alter basal 5'-nucleotidase activity. However, it prevented stimulation by 5 microM dipyridamole. Adenosine availability at the receptor sites was increased by dipyridamole and S-(p-nitrobenzyl)-6-thioinosine (NBTI), which inhibit adenosine uptake into the cell. Addition of dipyridamole or NBTI to the adenosine-treated mesangial cells produced an additive increase in ecto-5'-nucleotidase activity. Dipyridamole, through its effect on extracellular adenosine and ecto-5'-nucleotidase, may have an influence upon regulation of the glomerular microcirculation.
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PMID:Effect of dipyridamole on glomerular mesangial cell ecto-5'-nucleotidase expression. 795 70