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Titolo:
EFFECT OF AN ENDOTHELIN-RECEPTOR ANTAGONIST ON ISCHEMIC ACUTE-RENAL-FAILURE
Autore:
CHAN L; CHITTINANDANA A; SHAPIRO JI; SHANLEY PF; SCHRIER RW;
Indirizzi:
UNIV COLORADO,HLTH SCI CTR,SCH MED,DEPT MED,BOX C281,4200 E NINE AVE DENVER CO 80262
Titolo Testata:
The American journal of physiology
fascicolo: 1, volume: 266, anno: 1994,
parte:, 2
pagine: 60000135 - 60000138
SICI:
0002-9513(1994)266:1<60000135:EOAEAO>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERFUSED RAT-KIDNEY; INVIVO; CELLS;
Keywords:
ENDOTHELIN RECEPTORS; ENDOTHELIN ANTAGONIST; ISOLATED KIDNEY PERFUSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
22
Recensione:
Indirizzi per estratti:
Citazione:
L. Chan et al., "EFFECT OF AN ENDOTHELIN-RECEPTOR ANTAGONIST ON ISCHEMIC ACUTE-RENAL-FAILURE", The American journal of physiology, 266(1), 1994, pp. 60000135-60000138

Abstract

In the isolated perfused rat kidney, endothelin (ET) added to the perfusate at concentrations ranging from 50 to 500 pmol/l resulted in a dose-dependent reduction in renal perfusate flow (RPF) and inulin clearance (C-In). The decrease in RPF (17 +/- 3 vs. 34 +/- 3 ml.min(-1).g(-1); P < 0.01 compared with control) and C-In (89 +/- 13 vs. 317 +/- 19mu l.min(-1).g(-1); P < 0.01 compared with control) by ET (500 pmol/l) was prevented by the ET antagonist BQ-123 (10 mu M), with full recovery of RPF [36 +/- 2 vs. 34 +/- 3 ml.min(-1).g(-1); not significant (NS) compared with control] and C-In (299 +/- 51 vs. 317 +/- 19 mu L.min(-1).g(-1); NS compared with control). In the absence of ET, perfusionof the kidney with a similar concentration of BQ-123 (10 mu M) did not induce any changes in RPF (36 +/- 5 vs. 34 +/- 3 ml.min(-1).g(-1); NS compared with control) or C-IN (320 +/- 14 vs. 317 +/- 19 mu l.min(-1).g(-1); NS compared with control). After 60 min of arterial clamping, BQ-123 (10 mu M) given before the onset of ischemia and during reflow improved C-IN (88 +/- 4 vs. 19 +/- 3 mu l.min(-1).g(-1); n = 6, P < 0.01) and net tubular sodium reabsorption (T-Na) compared with no treatment. On the other hand, the same dose (10 mu M) of BQ-123 given onlyduring the reperfusion period was not effective in preventing the decreases in either C-In or T-Na. Further studies were then performed to study the in vivo effect of BQ-123 in ischemic acute renal failure. Renal ischemia was induced by bilateral renal artery clamp for 45 min. BQ-123 (0.5 mg.kg(-1) min(-1) iv) or vehicle was infused both 30 min before clamping and during the 60-min reperfusion period. Treatment withBQ-123 resulted in significantly better C-In (1,310 +/- 50 vs. 590 +/- 85 mu l.min at 2 h; 1,920 +/- 160 vs. 810 +/- 90 mu l/min at 48 h ofreflow) and T-Na (175 +/- 15 vs. 80 +/- 10 mu l/min at 2 h; 270 +/- 15 vs. 110 +/- 10 mu l/min at 48 h of reflow) compared with vehicle. The effect of BQ-123 on the severity of injury in the S3 segment of the proximal tubule 48 h after ischemia was also found to be significantlyless in the treated group. These results therefore suggest that BQ-123, the ET-receptor antagonist, is potentially an important agent in the prevention of ischemic acute renal failure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 23:13:16