PMID: 8957538Jan 1, 1996Paper

Altered inotropism in the failing human myocardium

Basic Research in Cardiology
U BavendiekR H Schwinger

Abstract

Beta-adrenoreceptor-cAMP-dependent inotropic interventions lose their effectiveness depending on the degree of myocardial failure. This blunted effect of beta-adrenoreceptor-dependent stimulation might be due to a downregulation of beta-adrenoreceptors and an increase of inhibitory G-proteins leading to decreased intracellular cAMP-concentrations. However, the maximal positive inotropic effect elicited by elevation of the extracellular [Ca2+] does not differ between failing and nonfailing human myocardium, indicating that terminally failing human myocardium is effective to increase force of contraction to the same degree as nonfailing tissue. Agents which increase force of contraction primarily via increasing the intracellular [Na+], e.g., cardiac glycosides and the Na(+)-channel activator BDF 9148, exert a higher potency in failing myocardium than in nonfailing tissue to increase force of contraction. This could result from an enhanced protein expression of the Na+/Ca(2+)-exchanger observed in diseased human hearts. Alterations in the intracellular Ca(2+)-homeostasis reported in failing myocardium lead to a negative force-frequency-relationship and a prolonged relaxation. As the protein expression of SERCA IIa and phospholamba...Continue Reading

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Citations

Jan 22, 2004·Journal of Molecular and Cellular Cardiology·Eric I RossmanKenneth B Margulies
Jan 22, 2004·Journal of Molecular and Cellular Cardiology·E G Lakatta
Jun 28, 2008·The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation·Pippa M SchneeRoger J Bick
Apr 12, 2001·Cytokine·K M Kulmatycki, F Jamali
Jun 6, 1998·Cardiovascular Research·R M PhillipsR A Altschuld
Nov 16, 2018·Genome Biology·Maja P Mattle-GremingerMichael Krützen

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