AMP deaminase, 5′-nucleotidase and adenosine deaminase in rat myocardial tissue in myocardial infarction and hypothermia

Saleem, Yousuf; Niveditha, T.; Sadasivudu, B.

doi:10.1007/bf01972265

Cited by 9 publications

(3 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another possibility is that ischemic conditions could change the activities of adenosine kinase and/or adenosine deaminase. Studies performed in rats subjected to experimental myocardial infarction have demonstrated that adenosine deaminase activity is significantly increased in infarcted tissue (33). It has also been shown that global ischemia for 10 min significantly elevates adenosine deaminase activity in the rat heart (8).…”

Section: Discussionmentioning

confidence: 99%

Renal interstitial adenosine metabolism during ischemia in dogs

Nishiyama¹,

Kimura²,

He³

et al. 2001

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

The present study was conducted to determine the metabolism of renal interstitial adenosine under resting conditions and during ischemia. By using a microdialysis method with HPLC-fluorometric analysis, renal interstitial concentrations of adenosine, inosine, and hypoxanthine were assessed in pentobarbital-anesthetized dogs. Average basal renal interstitial concentrations of adenosine, inosine, and hypoxanthine were 0.18 +/- 0.04, 0.31 +/- 0.05, and 0.35 +/- 0.05 micromol/l, respectively. Local inhibition of adenosine kinase with iodotubercidin (10 micromol/l in perfusate) or inhibition of adenosine deaminase with erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; 100 micromol/l in perfusate) did not change adenosine concentrations in the nonischemic kidneys (0.18 +/- 0.04 and 0.24 +/- 0.05 micromol/l, respectively). On the other hand, treatment with iodotubercidin+EHNA significantly increased adenosine concentration (0.52 +/- 0.07 micromol/l) with significant decreases in inosine and hypoxanthine levels (0.13 +/- 0.03 and 0.19 +/- 0.04 micromol/l, respectively). During 30 min of ischemia, adenosine, inosine, and hypoxanthine were significantly increased to 0.76 +/- 0.29, 2.14 +/- 0.45, and 21.8 +/- 4.7 micromol/l, respectively. The treatment with iodotubercidin did not alter ischemia-induced increase in adenosine (0.84 +/- 0.18 micromol/l); however, EHNA alone markedly enhanced adenosine accumulation (13.54 +/- 2.16 micromol/l), the value of which was not augmented by an addition of iodotubercidin (15.80 +/- 1.24 micromol/l). In contrast, ischemia-induced increases in inosine and hypoxanthine were inversely diminished by the treatment with iodotubercidin+EHNA (0.90 +/- 0.20 and 9.86 +/- 1.96 micromol/l, respectively). These results suggest that both adenosine kinase and adenosine deaminase contribute to the metabolism of renal interstitial adenosine under resting conditions, whereas adenosine produced during ischemia is mainly metabolized by adenosine deaminase and the rephosphorylation of adenosine by adenosine kinase is small.sent

show abstract

Section: Discussionmentioning

confidence: 99%

Renal interstitial adenosine metabolism during ischemia in dogs

Nishiyama¹,

Kimura²,

He³

et al. 2001

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…Thus, the bimolecular complex of DPP‐4 and ADA catalyses the irreversible deamination of adenosine to inosine in the purine catabolic pathway and increases uric acid and superoxide anions as end‐products . ADA activity is increased in myocardial tissues after myocardial infarction (MI) . Although ADA blockers have been reported to decrease radical generation and prevent postischemic heart injury , there were controversies regarding the cardioprotection of ADA blockers.…”

Section: Introductionmentioning

confidence: 99%

Sitagliptin attenuates sympathetic innervation via modulating reactive oxygen species and interstitial adenosine in infarcted rat hearts

Lee

Chen

Yang

et al. 2014

J Cellular Molecular Medi

View full text Add to dashboard Cite

We investigated whether sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, attenuates arrhythmias through inhibiting nerve growth factor (NGF) expression in post-infarcted normoglycemic rats, focusing on adenosine and reactive oxygen species production. DPP-4 bound adenosine deaminase has been shown to catalyse extracellular adenosine to inosine. DPP-4 inhibitors increased adenosine levels by inhibiting the complex formation. Normoglycemic male Wistar rats were subjected to coronary ligation and then randomized to either saline or sitagliptin in in vivo and ex vivo studies. Post-infarction was associated with increased oxidative stress, as measured by myocardial superoxide, nitrotyrosine and dihydroethidium fluorescent staining. Measurement of myocardial norepinephrine levels revealed a significant elevation in vehicle-treated infarcted rats compared with sham. Compared with vehicle, infarcted rats treated with sitagliptin significantly increased interstitial adenosine levels and attenuated oxidative stress. Sympathetic hyperinnervation was blunted after administering sitagliptin, as assessed by immunofluorescent analysis and western blotting and real-time quantitative RT-PCR of NGF. Arrhythmic scores in the sitagliptin-treated infarcted rats were significantly lower than those in vehicle. Ex vivo studies showed a similar effect of erythro-9-(2-hydroxy-3-nonyl) adenine (an adenosine deaminase inhibitor) to sitagliptin on attenuated levels of superoxide and NGF. Furthermore, the beneficial effects of sitagliptin on superoxide anion production and NGF levels can be reversed by 8-cyclopentyl-1,3-dipropulxanthine (adenosine A1 receptor antagonist) and exogenous hypoxanthine. Sitagliptin protects ventricular arrhythmias by attenuating sympathetic innervation via adenosine A1 receptor and xanthine oxidase-dependent pathways, which converge through the attenuated formation of superoxide in the non-diabetic infarcted rats.

show abstract

“…The activity of 5'-nucleotidase in cardiac tissue is known to change according to the physiological state of the cell (29), during aging (12), in hypertrophy (26), and Saleem et al (30) have reported a decrease in the activity of 5'-nucleotidase in the left ventricle after 90 rain of ischaemia. Recently we reported fourfold differences between the atria and ventricles in the activity of this enzyme in the normal canine heart (9).…”

Section: Introductionmentioning

confidence: 98%

Differences in the regional distribution and response to ischaemia of adenosine-regulating enzymes in the heart

Choong

Humphrey

1987

Basic Res Cardiol

View full text Add to dashboard Cite

The activities of the adenosine-generating enzyme 5'-nucleotidase and the adenosine-degrading enzyme adenosine deaminase were determined for four regions of rat hearts prior to and following 10-60 min of ischaemia. Whereas adenosine deaminase was uniformly active throughout the heart, 5'-nucleotidase was twice as active in atrial than in ventricular myocardium, and more active in the right than in the left ventricles in normoxic tissues. In isolated heart preparations normoxic perfusion decreased adenosine deaminase and increased 5'-nucleotidase activity compared to levels in vivo. Global ischaemia for 10 min elevated adenosine deaminase activity but had no effect on 5'-nucleotidase activity. However, 30 min of ischaemia decreased 5'-nucleotidase activity by 50% in all regions of the heart. These changed levels were not altered by 10 min of reperfusion. The fall in 5'-nucleotidase activity with ischaemia occurred only in the 90% of this enzyme which is membrane-bound. The reasons for the marked differences in distribution and responses to ischaemia of these two enzymes have yet to be elucidated but metabolic inhibitors seem unlikely to be involved.

show abstract

AMP deaminase, 5′-nucleotidase and adenosine deaminase in rat myocardial tissue in myocardial infarction and hypothermia

Cited by 9 publications

References 9 publications

Renal interstitial adenosine metabolism during ischemia in dogs

Renal interstitial adenosine metabolism during ischemia in dogs

Sitagliptin attenuates sympathetic innervation via modulating reactive oxygen species and interstitial adenosine in infarcted rat hearts

Differences in the regional distribution and response to ischaemia of adenosine-regulating enzymes in the heart

Contact Info

Product

Resources

About