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Titolo:
Endothelin and endothelin A/B receptors are increased after ischaemic acute renal failure
Autore:
Forbes, JM; Jandeleit-Dahm, K; Allen, TJ; Hewitson, TD; Becker, GJ; Jones, CL;
Indirizzi:
Royal Childrens Hosp, Dept Nephrol, Victorian Paediat Renal Serv, Parkville, Vic 3052, Australia Royal Childrens Hosp Parkville Vic Australia 3052 le, Vic 3052, Australia Univ Melbourne, Austin Repatriat Med Ctr, Dept Med, Heidelberg, Vic, Australia Univ Melbourne Heidelberg Vic Australia Med, Heidelberg, Vic, Australia Royal Melbourne Hosp, Dept Nephrol, Parkville, Vic 3050, Australia Royal Melbourne Hosp Parkville Vic Australia 3050 le, Vic 3050, Australia
Titolo Testata:
EXPERIMENTAL NEPHROLOGY
fascicolo: 5, volume: 9, anno: 2001,
pagine: 309 - 316
SICI:
1018-7782(2001)9:5<309:EAEARA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; RAT; CELLS; LOCALIZATION; ANTAGONISTS; MACROPHAGES; SUBTYPE; MONOCYTES; SB-209670; REVERSAL;
Keywords:
endothelin; acute renal failure; ischaemia; endothelin receptors; renal medullary interstitial cell;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Jones, CL Royal Childrens Hosp, Dept Nephrol, Victorian Paediat Renal Serv, Flemington Rd, Parkville, Vic 3052, Australia Royal Childrens Hosp Flemington Rd Parkville Vic Australia 3052
Citazione:
J.M. Forbes et al., "Endothelin and endothelin A/B receptors are increased after ischaemic acute renal failure", EXP NEPHROL, 9(5), 2001, pp. 309-316

Abstract

Background/Aims: Endothelin (ET) has been implicated as an indirect mediator of injury following acute renal ischaemia (ARI). The purpose of this study was to localize and quantitate ET and ETA and ETB receptors following ARL Methods: A model of ARI, well characterized previously, was produced by 45 min occlusion of the renal pedicle of unilaterally nephrectomized female Sprague-Dawley rats. Animals were sacrificed 1, 2, 4, 8, 16, 32 and 64 daysafter ischaemia (n = 6). Corresponding control groups with unilateral nephrectomy but no ischaemia were sacrificed after 0, 8 and 64 days. Immunohistochemistry for ET-1, -2 and -3 was performed. Tissue ET levels were calculated by RIA (femtomoles per kidney). Receptor ligand binding studies for ETAand ETB receptors were performed by autoradiography on frozen kidney sections and quantitated by densitometry (relative optical density per square millimetre). Results: The concentration of tissue ET increased from 24 h after ischaemia and remained significantly increased for the duration of the study, reaching a maximum at 8 days. There was a small increase in the non-ischaemic 8-day control group, but this returned to basal levels by day 64. The increase in tissue ET 8 days after ischaemia was localized by immunohistochemistry to renal medullary interstitial cells, damaged tubules at the corticomedullary junction and peritubular capillaries surrounding these damaged tubules. Increases in cortical ETA and ETB receptors were evident 24 h after ischaemia and were maximal 8 days after ischaemia, before returning tobasal levels at 16 days. After a small increase 24 h after ischaemia, medullary ETA receptors decreased on day 4 before returning to basal levels on day 8 after ischaemia. Medullary ETB receptors, however, decreased on day 4after ischaemia and remained low throughout the duration of the study. Conclusion: The previously reported amelioration of pathological changes resulting from the use of ET receptor antagonists after ARI may be related to the quantitative and qualitative changes in tissue ET and ET receptors observed in this study. Copyright (C) 2001 S. Karger AG, Basel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 22:55:02