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Titolo:
The cardiac endothelin system in established pressure overload left ventricular hypertrophy
Autore:
Schunkert, H; Orzechowski, HD; Bocker, W; Meier, R; Riegger, GAJ; Paul, M;
Indirizzi:
Univ Regensburg, Klin & Poliklin Innere Med 2, D-8400 Regensburg, Germany Univ Regensburg Regensburg Germany D-8400 2, D-8400 Regensburg, Germany Free Univ Berlin, Inst Clin Pharmacol & Toxicol, Benjamin Franklin Med Ctr, Berlin, Germany Free Univ Berlin Berlin Germany jamin Franklin Med Ctr, Berlin, Germany
Titolo Testata:
JOURNAL OF MOLECULAR MEDICINE-JMM
fascicolo: 8, volume: 77, anno: 1999,
pagine: 623 - 630
SICI:
0946-2716(199908)77:8<623:TCESIE>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONGESTIVE-HEART-FAILURE; ANGIOTENSIN-CONVERTING ENZYME; RAT-HEART; EXPRESSION; CARDIOMYOCYTES; INDUCTION; GENES;
Keywords:
cardiac hypertrophy; endothelin; endothelin converting enzyme; endothelin receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Schunkert, H Univ Regensburg, Klin & Poliklin Innere Med 2, D-8400 Regensburg, Germany Univ Regensburg Regensburg Germany D-8400 gensburg, Germany
Citazione:
H. Schunkert et al., "The cardiac endothelin system in established pressure overload left ventricular hypertrophy", J MOL MED-J, 77(8), 1999, pp. 623-630

Abstract

In normal hearts, endothelin-1 (ET-1) has been shown to initiate myocyte growth and to modulate cardiac function. However, regulation of the various components of the system and the functional effects of ET-1 in established left ventricular hypertrophy (LVH) are less clear. We thus studied ET-1, ETA receptor, and endothelin converting enzyme (ECE-1) mRNA regulation as well as the effects of ET-1 on coronary resistance, LV contractility and relaxation in hypertrophied rat hearts. Cardiac pressure overload, secondary to banding of the ascending aorta, resulted in a transient increase of cardiacET-1 and ETA receptor mRNAs that reached a maximum at 2 days (+75% and +40%, respectively, P<0.05, each). ET-1 mRNA levels reached a second peak at 84 days of pressure overload (+60%, P<0.05), at the later time point in conjunction with elevated ECE-1 mRNA levels (+20%, P<0.05). The functional implications of ET-1 were examined in a study of isolated perfused hearts. Bothhearts with established LVH and sham control hearts responded to ET-1 perfusion (10-(11) to 10(-9) M) with an increase of coronary perfusion pressure(CPP; +85+/-15 and +75+/-8 mmHg; P<0.001 each) and a slight decrease of LVsystolic pressure (LVP; -12+/-9 and -9+/-7 mmHg; P=NS). In contrast, ET-1 increased LV end-diastolic pressure (LVEDP) only in LVH hearts (+22+/-7 mmHg, P<0.05 versus baseline and +20 +/-7 mmHg, P<0.05 versus sham). Direct stimulation of protein kinase C mimicked the effects of ET-1, whereas inhibition of this kinase or the Na+-H+ exchanger blunted the effects of ET-1 on CPP, LVP, and LVEDP. Interestingly, coadministration of the vasodilator and the nitric oxide (NO) donor nitroglycerin not only prevented the increase of CPP and LVEDP, but also uncovered a slight positive inotropic effect of ET-1 in LVH hearts. Thus, the cardiac expression of ET-1, ETA, and ECE-1 mRNAs displays a distinct pattern during early and advanced cardiac pressure overload. Furthermore, ET-1 mediates a slight depression of systolic, and a profound depression of diastolic, functional parameters in hearts with established LVH, effects that appear to be secondary to ET-1-related coronary vasoconstriction. The data suggest a functional role of the endothelin system in hearts with established pressure overload hypertrophy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:55:15