Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Renal interstitial adenosine metabolism during ischemia in dogs
Autore:
Nishiyama, A; Kimura, S; He, H; Miura, K; Rahman, M; Fujisawa, Y; Fukui, T; Abe, Y;
Indirizzi:
Kagawa Med Univ, Dept Pharmacol, Miki, Kagawa 7610793, Japan Kagawa Med Univ Miki Kagawa Japan 7610793 ol, Miki, Kagawa 7610793, Japan Kagawa Med Univ, Res Equipment Ctr, Miki, Kagawa 7610793, Japan Kagawa MedUniv Miki Kagawa Japan 7610793 tr, Miki, Kagawa 7610793, Japan Osaka City Univ, Sch Med, Dept Pharmacol, Osaka 5458585, Japan Osaka City Univ Osaka Japan 5458585 Dept Pharmacol, Osaka 5458585, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: F231 - F238
SICI:
0363-6127(200102)280:2<F231:RIAMDI>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
A(1) RECEPTOR ANTAGONIST; BLOOD-FLOW; PURINE METABOLITES; INITIATION PHASE; RAT-KIDNEY; INHIBITION; KINASE; HEMODYNAMICS; FAILURE; MICROVASCULATURE;
Keywords:
renal interstitium; adenosine deaminase; adenosine kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Abe, Y Kagawa Med Univ, Dept Pharmacol, 1750-1 Ikenobe, Miki, Kagawa 7610793, Japan Kagawa Med Univ 1750-1 Ikenobe Miki Kagawa Japan 7610793 793, Japan
Citazione:
A. Nishiyama et al., "Renal interstitial adenosine metabolism during ischemia in dogs", AM J P-REN, 280(2), 2001, pp. F231-F238

Abstract

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 concentrationsof adenosine, inosine, and hypoxanthine were 0.18 +/- 0.04, 0.31 +/- 0.05,and 0.35 +/- 0.05 mu mol/l, respectively. Local inhibition of adenosine kinase with iodotubercidin (10 mu mol/l in perfusate) or inhibition of adenosine deaminase with erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; 100 mu mol/lin perfusate) did not change adenosine concentrations in the nonischemic kidneys (0.18 +/- 0.04 and 0.24 +/- 0.05 mu mol/l, respectively). On the other hand, treatment with iodotubercidin+EHNA significantly increased adenosine concentration (0.52 +/- 0.07 mu mol/l) with significant decreases in inosine and hypoxanthine levels (0.13 +/- 0.03 and 0.19 +/- 0.04 mu mol/l, respectively). During 30 min of ischemia, adenosine, inosine, and hypoxanthinewere significantly increased to 0.76 +/- 0.29, 2.14 +/- 0.45, and 21.8 +/-4.7 mu mol/l, respectively. The treatment with iodotubercidin did not alter ischemia-induced increase in adenosine (0.84 +/- 0.18 mu mol/l); however,EHNA alone markedly enhanced adenosine accumulation (13.54 +/- 2.16 mu mol/l), the value of which was not augmented by an addition of iodotubercidin (15.80 +/- 1.24 mu mol/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 mu mol/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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 20:31:00