Altered responsiveness to endothelin-1 of myocardium from pacing-induced heart failure model in the dog.

摘要: In congestive heart failure, in addition to a compensatory increase neurohumoral activation, there is an the endothelial-derived vasoconstrictive and positive inotropic substance, endothelin. Whether downregulation of cardiac effects this substance occurs, as has been shown occur with beta- alpha-adrenergic agonists, remains unknown. study we investigated endothelin-1 [dose-response curve (10-11 10-7 M)] on contractile characteristics isolated papillary muscles from normal dogs failure induced by pacing overdrive, or without removing endocardial endothelium muscles. Endothelin-1 caused similar absolute myocardial indices all four groups, except for shortening, which increased more endothelium. However, intact endothelium, relative was greater overdrive (failing) compared (tension 110% vs. 53%, p<0.01 shortening 127% 24%, p<0.01). Also, failing began responding at lower concentrations (10-10 10-9 M) than Endocardial endothelial removal endothelin-1, whether done myocardium. This thus indicates that, contrast other substances, model sensitivity response endothelin-1. It also that although increases both myocardium, responsiveness myocardium not dependent.