Ecto-5′-Nucleotidase Mediates Infarct Size-Limiting Effect by Ischemic Preconditioning in the Rabbit Heart

Komamura, Kazuo; Kitakaze, Masafumi; Funaya, Hiroharu; Ueda, Yasunori; Node, Koichi; Minamino, Tetsuo; Kurihara, Takushi; Hori, Masatsugu

doi:10.1097/00005344-199712000-00012

Cited by 7 publications

(5 citation statements)

References 40 publications

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“…Previous studies showed that 5Ј-ND was activated during myocardial ischemia and/or reperfusion and that increased production of adenosine in the myocardial tissue counteracted the cell injury under these circumstances (1,24,25). Inhibition of 5Ј-ND largely increased myocardial infarction induced by a 30-min coronary occlusion and 3-h reperfusion (24). These results support the view that enhanced 5Ј-ND activity protects the tissues or cells from the ischemic injury in the myocardium.…”

Section: Discussionsupporting

confidence: 77%

“…Given that adenosine can reduce glomerular filtration rate, decrease tubular loading, inhibit tubular ion transport activity, and increase medullary blood perfusion (41,48), this oxidant-induced increase in 5Ј-ND activity or adenosine production may represent an important adaptive mechanism during oxidative stress under pathological conditions such as ischemia and/or reperfusion (1,2,6). Previous studies showed that 5Ј-ND was activated during myocardial ischemia and/or reperfusion and that increased production of adenosine in the myocardial tissue counteracted the cell injury under these circumstances (1,24,25). Inhibition of 5Ј-ND largely increased myocardial infarction induced by a 30-min coronary occlusion and 3-h reperfusion (24).…”

Section: Discussionmentioning

confidence: 99%

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Oxidative stress enhances the production and actions of adenosine in the kidney

Chen

Zou

2001

American Journal of Physiology-Regulatory, Integrative and Comp

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The purpose of this study was to determine whether superoxide anions (O.) activate 5'-nucleotidase (5'-ND), thereby increasing the production of renal adenosine and regulating renal function. Using HPLC analysis, we found that incubation of renal tissue homogenate with the O. donor KO(2) doubled adenosine production and increased the maximal reaction velocity of 5'-ND from 141 to 192 nmol. min(-1). mg protein(-1). The O.-generating system, xanthine/xanthine oxidase increased the maximal reaction velocity of 5'-ND from 122 to 204 nmol. min(-1). mg protein(-1). Superoxide dismutase (SOD) with catalase produced a concentration-dependent reduction of 5'-ND activity in renal tissue homogenate, while the SOD inhibitor diethyldithiocarbamic acid significantly increased 5'-ND activity. Inhibition of disulfide bond formation by thioredoxin or thioredoxin reductase significantly decreased xanthine/xanthine oxidase-induced activation of renal 5'-ND. In in vivo experiments, inhibition of SOD by diethyldithiocarbamic acid (0.5 mg. kg(-1). min(-1) iv) enhanced renal vasoconstriction induced by endogenously produced adenosine and increased renal tissue adenosine concentrations under control condition and in ischemia and reperfusion. We conclude that oxidative stress activates 5'-ND and increases adenosine production in the kidney and that this redox regulatory mechanism of adenosine production is important in the control of renal vascular tone and glomerular perfusion.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Oxidative stress enhances the production and actions of adenosine in the kidney

Chen

Zou

2001

American Journal of Physiology-Regulatory, Integrative and Comp

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“…We further contemplated that our previous observation about elevation of e-AMP level that could not be explained by the unchanged level of ecto-5 0 -nucleotidase app 18 was possibly due to provoked induction of 5 0 -nucleotidase app activity in the blood vessels as already demonstrated in several studies. [50][51][52] In addition, Komamura et al 53 showed that ecto-5 0 -nucleotidase activity in ischemic region of rabbit heart following ischemic preconditioning was greater than that in nonischemic regions. In addition, decrease in ecto-adenosine deaminase app activity raises the level of e-AMP.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Purine Metabolism in Blood Vessels (Part II): Activity of Ecto-Enzymes in Blood Vessels of Patients With Abdominal Aortic Aneurysm

Lecka

Bloch-Bogusławska

Molski

et al. 2010

Clin Appl Thromb Hemost

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Both platelet aggregation and high blood pressure are associated with development of atherosclerosis. Among other factors that modulate platelet aggregation and blood pressure, extracellular purines (e-purines) influence these processes via purinoceptors P1 and P2 for which they are natural ligands. We hypothesized that ecto-enzymes such as nucleoside triphosphate diphosphohydrolases (NTPDases), adenylate kinase, 5'-nucleotidase, and adenosine deaminase that regulate the level of e-purines may be involved in the development of atherosclerosis. The enzymatic assays were performed either on the fragments of human abdominal aortas obtained after death or on abdominal aneurysm samples collected during surgery. The substrates and products such as adenine nucleosides and nucleotides were analyzed using reverse phase high-performance liquid chromatography (HPLC) method. Here, we estimated and demonstrated the activities of these ecto-enzymes in the patients with atherosclerosis or atherosclerosis-like diseases such as abdominal aneurysm, myocardial infarction, or Leriche syndrome (LS) with worse thrombosis of extremities. In particular, we noticed reduction in activity of NTPDase1(app), NTPDase2(app), ecto-adenylate kinase( app), and ecto-adenosine deaminase(app); however, ecto-5'-nucleotidase(app) that hydrolyzed e-adenosine monophosphate (e-AMP) into e-adenosine did not show any significant changes. This led us to suggest that alteration of the activity of examined ecto-enzymes is responsible for the development of atherosclerosis or atherosclerosis-like diseases.

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“…After surgery, the preparation was equilibrated for 90 min to allow the stabilization of the interstitial adenosine concentration before the collection of samples was begun. Additional studies were performed to evaluate the effect of the blockade of 5Ј-ND on interstitial adenosine by infusing ␣,␤-mADP at 0.00105 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 into the aorta (6,23). The dose used induced the smaller changes in MAP and urinary flow compared with several tested doses (data not shown), including the 0.035 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 previously described (6).…”

Section: Renal Interstitial Concentration Of Adenosinementioning

confidence: 99%

Renal interstitial adenosine is increased in angiotensin II-induced hypertensive rats

Franco¹,

Bautista²,

Pérez-Méndez³

et al. 2008

American Journal of Physiology-Renal Physiology

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Since marked renal vasoconstriction is observed in angiotensin II (ANG II)-mediated hypertensive rats, we studied the possible interaction between ANG II and adenosine in this model. ANG II was infused into male Wistar rats through osmotic minipumps (435 ng x kg(-1) x min(-1)) for 14 days. In sham and ANG II groups, renal tissue and interstitial adenosine were measured; both increased to a similar twofold extent in the ANG II-treated rats (31.40 +/- 4 vs. 62.0 +/- 8.4 nM, sham vs. ANG II, interstitial adenosine; P< 0.001). The latter decreased by 47% with the specific blockade of 5'-nucleotidase. Glomerular hemodynamics demonstrated marked renal vasoconstriction in the angiotensin-treated group, which was reverted by an adenosine A(1)-receptor antagonist (8-cyclopentyl-1,3-dipropylxanthine, 10 mug.kg(-1) x min(-1)). 5'-Nucleotidase and adenosine deaminase (ADA) activities were measured in the cytosolic and membrane fractions. Only the membrane ADA activity decreased from 1,202 +/- 80 to 900 +/- 50 mU/mg protein in the ANG II-treated rats (P< 0.05), as well as in their protein and mRNA expression. Despite the adenosine elevation, A(1) and A(2b) receptor protein did not change; in contrast, downregulation was observed in A(2a) receptor and upregulation in A(3) receptor. A similar pattern was found in the cortex and in the medulla; mRNA significantly decreased only in the A(3) receptor in both segments. These results suggest that the elevation of renal tissue and interstitial adenosine contributes to the renal vasoconstriction observed in the ANG II-induced hypertension and that it is mediated by a decrease in the activity and expression of ADA, increased production of adenosine, and an induced imbalance in adenosine receptors.

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Ecto-5′-Nucleotidase Mediates Infarct Size-Limiting Effect by Ischemic Preconditioning in the Rabbit Heart

Cited by 7 publications

References 40 publications

Oxidative stress enhances the production and actions of adenosine in the kidney

Oxidative stress enhances the production and actions of adenosine in the kidney

Extracellular Purine Metabolism in Blood Vessels (Part II): Activity of Ecto-Enzymes in Blood Vessels of Patients With Abdominal Aortic Aneurysm

Renal interstitial adenosine is increased in angiotensin II-induced hypertensive rats

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