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)

It has been reported recently that adenosine and ATP produce dose- and tone-dependent responses in the feline pulmonary vascular (PV) bed. The present study was undertaken to investigate the mechanisms mediating vasoconstrictor (VC) responses to adenosine and ATP in the intact-chest, spontaneously breathing cat under conditions of controlled blood flow and constant left atrial pressure. The order of potency of adenosine receptor agonists to produce VC in the PV bed was the selective adenosine A1 receptor agonist R-phenylisopropyladenosine greater than the mixed A1, A2 receptor agonist, adenosine greater than the selective adenosine A2 receptor agonist, 2-phenylaminoadenosine. The dose-related increase in lobar arterial pressure in response to adenosine was blocked by an adenosine (P1) receptor antagonist, BWA1433U, the cyclooxygenase inhibitor, meclofenamate, and the thromboxane A2 receptor antagonist, SQ29548. The order of potency of ATP analogs to produce VC in the PV bed was alpha,beta-methylene ATP (alpha,beta-meATP) much greater than beta,tau-methylene ATP greater than ATP. BWA1433U inhibited VC responses to ATP without affecting responses to its degradation-resistant analogs beta,tau-methylene ATP and alpha,beta-meATP. In the presence of BWA1433U and a continuous intralobar infusion of the selective 5'-nucleotidase inhibitor, alpha,beta-methyleneadenosine-5'-diphosphate, ATP VC responses are significantly enhanced compared to those after BWA1433U. alpha,beta-Methyleneadenosine-5'-diphosphate had no effect on the VC response to U44069 after BWA1433U. Meclofenamate significantly inhibited the vasoconstrictor responses to ATP but not to alpha,beta-meATP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine and ATP produce vasoconstriction in the feline pulmonary vascular bed by different mechanisms. 183 63

This study was undertaken to clarify factors other than nitric oxide involved in reactive hyperemia after a short (30 sec) and a long (300 sec) coronary global no-flow ischemia in isolated rat hearts perfused at a constant pressure (90 mmHg) with special focuses on the contribution of various K channels including large and small conductance Ca-activated K (KCa) channels as well as ATP-sensitive K (KATP) channels. Reactive hyperemia was induced following 30 sec and 300 sec of no-flow ischemia of the heart. Coronary reactive hyperemia was observed even after the inhibition of nitric oxide synthase by N(omega)-nitro-L-arginine methylester (L-NAME). Selected K channel blockers, none of which affected the basal flow, were used to evaluate contribution of K channels to this L-NAME-resistant reactive hyperemia. After 30-sec ischemia, tetraethylammonium (TEA: a non-selective K channel blocker), glibenclamide (Gli: a KATP channel blocker) and alpha,beta-methylene adenosine 5'-diphosphonate (AOPCP: an inhibitor of ecto 5'-nucleotidase) all suppressed both peak flow/basal flow (%PF) and repayment of flow debt (%RFD). After 300-sec ischemia, TEA and charybdotoxin (ChTX: a large conductance KCa channel blocker) decreased %PF and %RFD; AOPCP decreased both %RFD and duration, 4-aminopyridine (a voltage-dependent K channel blocker) decreased only duration. Neither apamin (a small conductance KCa channel blocker) nor indomethacin (a cyclooxygenase inhibitor) affected the both types of reactive hyperemia. These findings suggest that opening of KATP channel contributes to coronary vasodilation in reactive hyperemia after short 30-sec ischemia, and that opening of KCa, but not KATP, channel contributes to it after long 300-sec ischemia. These results also suggest that adenosine may partly be involved in both types of reactive hyperemia.
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PMID:Types of potassium channels involved in coronary reactive hyperemia depend on duration of preceding ischemia in rat hearts. 929 38

Experiments were performed to characterize renal hemodynamics in Thy-1 nephritic rats. A monoclonal antibody against Thy-1 was intravenously injected to induce mesangiolysis in rats, and 2 days later renal hemodynamic responses to variations in blood pressure were determined. In the first series of experiments, autoregulation of renal plasma flow (RPF) or glomerular filtration rate (GFR) was impaired in nephritic rats. In response to a reduction in blood pressure (98 +/- 2 to 80 +/- 1 mmHg), both RPF (4.17 +/- 0.63 to 3.20 +/- 0.45 ml x min(-1) x g kidney wt(-1), P < 0.05, n = 6) and GFR (0.88 +/- 0.05 to 0.75 +/- 0.06 ml x min(-1).g kidney wt(-1), P < 0.05) were decreased in nephritic rats. Intravenous administration of furosemide and 30% albumin, both of which inhibit tubuloglomerular feedback, diminished renal autoregulation in control but not nephritic rats. In the second studies, the infusion of 5'-nucleotidase, an enzyme expressed on mesangial cells, into a renal artery ameliorated the magnitude of autoregulatory decrements in GFR in nephritic rats (-16 +/- 5 to -6 +/- 2%, P < 0.05, n = 6), but this enzyme failed to alter renal autoregulation in control rats. In the third studies, the effects of indomethacin were examined in nephritic rats. Inhibition of prostaglandin synthesis reduced RPF (4.07 +/- 0.30 to 1.54 +/- 0.22 ml x min(-1) x g kidney wt(-1), P < 0.05, n = 5) and GFR (1.03 +/- 0.18 to 0.69 +/- 0.13 ml x min(-1) x g kidney wt(-1), P < 0.05) in nephritic rats. However, cyclooxygenase inhibition failed to restore renal autoregulation in nephritic rats. Our results indicate that renal autoregulation is impaired in Thy-1 nephritis. Furthermore, the present data provide evidence that prostanoids contribute to maintain renal circulation in nephritic rats. Finally, our findings suggest that mesangial cells and/or 5'-nucleotidase plays an important role in mediating renal autoregulation.
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PMID:Exogenous 5'-nucleotidase improves glomerular autoregulation in Thy-1 nephritic rats. 1618 93