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Titolo:
Contribution of the endothelin system to the renal hypoperfusion associated with experimental congestive heart failure
Autore:
Friedrich, EB; Muders, F; Luchner, A; Dietl, O; Riegger, GAJ; Elsner, D;
Indirizzi:
Univ Regensburg, Klin & Poliklin Innere Med 2, Regensburg, Germany Univ Regensburg Regensburg Germany in Innere Med 2, Regensburg, Germany
Titolo Testata:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
fascicolo: 4, volume: 34, anno: 1999,
pagine: 612 - 617
SICI:
0160-2446(199910)34:4<612:COTEST>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASOCONSTRICTOR PEPTIDE; A RECEPTOR; EXPRESSION; POTENT; INHIBITION; MEDICINE; BLOCKADE;
Keywords:
heart failure; renal hemodynamics; rabbit-endothelin-1; ETA receptor; BQ-123;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Friedrich, EB Univ Klinikum Regensburg, Klin & Poliklin Innere Med 2, Franz Josef Str Allee 11, D-93042 Regensburg, Germany Univ Klinikum Regensburg Franz Josef Str Allee 11 Regensburg Germany D-93042
Citazione:
E.B. Friedrich et al., "Contribution of the endothelin system to the renal hypoperfusion associated with experimental congestive heart failure", J CARDIO PH, 34(4), 1999, pp. 612-617

Abstract

The objective of this study was to define further the local activation of endothelin-1 (ET-1) and the ETA receptor as well as the functional consequences of activated ET-1 for renal hypoperfusion associated with experimentalcongestive heart failure (CHF). We studied eight rabbits permanently instrumented with Doppler flow probes around the renal arteries before and afterthe induction of epinephrine-induced CHF. CHF was characterized by left-ventricular dysfunction (fractional shortening 34 +/- 2% vs. 46 +/- 3%; p less than or equal to 0.05) and dilatation (LVEDd 13.6 +/- 0.3 vs. 11.5 +/- 0.4 mm; p less than or equal to 0.05), decreased mean arterial pressure (59.4+/- 2.9 vs. 74.6 +/- 3.7 mm Hg; p less than or equal to 0.05), increased heart rate (236 +/- 11 vs. 216 +/- 8 beats/min; p less than or equal to 0.05) and renal vasoconstriction (vascular resistance 49.65 +/- 8.55 vs. 24.61 /- 5.85 U; p < 0.05; blood flow velocity, 1.58 +/- 0.21 vs. 3.63 +/- 0.31 kHz; p < 0.05). ET-1 concentrations were significantly increased not only in plasma (7.67 +/- 0.47 vs. 4.56 +/- 0.69 pg/ml; p < 0.05) but also in renal tissue (4.8 +/- 0.5 vs. 3.5 +/- 0.64 pg/mg; p < 0.05). Northern analysis revealed an unchanged expression of ETA receptor messenger RNA (0.79 +/- 0.05 vs. 0.77 +/- 0.04 arbitrary units; NS) in renal tissue, whereas expression of prepro-ET-1 was below the range of detection. In CHF, selective ETA-receptor antagonism with BQ-123 (1 mg/ kg bolus, i.v.) significantly increased renal blood flow velocity (3.07 +/- 0.38 vs. 1.33 +/- 0.19 kHz; p < 0.05) and reduced renal vascular resistance (29.63 +/- 6.22 vs. 58.17 +/- 8.75 U; p < 0.05) without significant effects on mean arterial pressure or heartrate. These studies demonstrate activation of the renal ET system, unaltered gene expression, and functional integrity of the renal ETA receptor in CHF. They indicate a principal functional role for the ETA receptor in renalvasoconstriction and suggest blockade of the renal ETA receptor as an important strategy to attenuate renal hypoperfusion in CHF.

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Documento generato il 05/04/20 alle ore 13:38:33