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Titolo:
Inotropic effects of endothelin-1 - Interaction with molsidomine and with BQ 610
Autore:
Beyer, ME; Slesak, G; Hovelborn, T; Kazmaier, S; Nerz, S; Hoffmeister, HM;
Indirizzi:
Univ Tubingen, Med Klin, Abt 3, D-72076 Tubingen, Germany Univ Tubingen Tubingen Germany D-72076 Abt 3, D-72076 Tubingen, Germany
Titolo Testata:
HYPERTENSION
fascicolo: 1, volume: 33, anno: 1999,
pagine: 145 - 152
SICI:
0194-911X(199901)33:1<145:IEOE-I>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL ENERGY-METABOLISM; NITRIC-OXIDE FORMATION; VASOCONSTRICTOR PEPTIDE; RAT-HEART; PLASMA ENDOTHELIN-1; ANESTHETIZED RAT; ANGINA-PECTORIS; ET(B) RECEPTOR; IN-VIVO; CONTRACTILITY;
Keywords:
endothelin; BQ 610; molsidomine; contractility; phosphates, high-energy; rats;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Beyer, ME Univrmanyngen, Med Klin, Abt 3, Otfried Muller Str 10, D-72076 Tubingen, Ge Univ Tubingen Otfried Muller Str 10 Tubingen Germany D-72076 Ge
Citazione:
M.E. Beyer et al., "Inotropic effects of endothelin-1 - Interaction with molsidomine and with BQ 610", HYPERTENSIO, 33(1), 1999, pp. 145-152

Abstract

In vivo studies could not detect a positive inotropy of endothelin (ET)-1 as described in in vitro experiments. ET-induced direct positive inotropy, which seems to be mediated by ETB receptors, may be antagonized in vivo by an indirect cardiodepressive effect owing to an ET-induced coronary vasoconstriction via ETA receptors. This study compares the effects of a dose of 1nmol/kg ET-1 alone on myocardial contractility and myocardial energy metabolism with the effects of I nmol/kg ET-I after pretreatment with 5 mg/kg molsidomine or with 100 mu g/kg of the ETA receptor antagonist BQ 610. We investigated the effects of ET-1 versus saline controls in open-chest rats. Inaddition to measurements in the intact circulation, myocardial function was examined by isovolumic registrations independent of peripheral vascular effects. We also studied the effect of ET-1 on myocardial high-energy phosphates. Pretreatment with molsidomine and BQ 610 attenuated the ET-induced reduction of cardiac output (ET-1: -62%; molsidomine+ET-1: -47%; BQ 610+ET-1:-27% different from controls). After a transient initial vasodilation, ET-1 raised total peripheral resistance (ET-1: +190%; molsidomine+ET-1: +171%;BQ 610+ET-1: +89%). BQ 610 was more effective in preventing ET-induced vasoconstriction. The increase of isovolumic peak first derivative of left ventricular pressure (ET-1: -2%; molsidomine+ET-1: +16%; BQ 610+ET-1: +19%) after pretreatment with molsidomine or BQ 610 indicates that these drugs unmask the positive inotropy of ET-1. ET-induced myocardial ischemia was abolished by molsidomine and BQ 610. Pretreatment with molsidomine or blockade ofETA receptors by BQ 610 can unmask the positive inotropy of ET-1 by preventing ET-induced myocardial ischemia. The positive inotropic effect of ET-1 seems to be mediated by ETB receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/05/20 alle ore 15:23:44