Schwinger Robert H. G.; Bohm, Michael; Erdmann, ErlandJournal of Cardiovascular Pharmacology: May 1990 Article: PDF Only Free Abstract Summary We investigated the “receptor-effectorcoupling” in the β-adrenoceptor- and the Na+, K +-ATPase-mediated systems in nonfailing hearts and terminally failing human myocardium from patients with cardiomyopathy. The density of β-adrenoceptors in the failing human myocardium was significantly (p < 0.01) lower as compared with nonfailing hearts, whereas the receptor density and affinity measured by [3H]ouabain binding (cardiac glycoside receptor) was not different in either group. The maximal inotropic response to isoprenaline was significantly reduced in papillary muscle strips from failing human hearts (2.1 ± 0.5 mN) as compared with control hearts (8.0 ± 1.0 mN; p < 0.05). Ouabain remained effective in both groups (6.8 ± 1.0 vs. 5.5 ± 0.6 mN; NS). The positive inotropic response due to extracellular Ca2+ elevation (1.8–15 mM) was studied for comparison. Maximal Ca2+ effects were reduced by 30% in failing human myocardium (7.2 ± 0.5 mN vs. 5.1 ± 0.8 mN, p < 0.05). Ouabain had effectiveness (95%) similar to that of Ca2+ in nonfailing and failing human cardiac muscle. It is concluded that treatment with cardiac glycosides may still be effective in end-stage heart failure with “downregulated” β-adrenoceptors, as judged from these in vitro studies. © Lippincott-Raven Publishers.