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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

In vitro comparative studies of the calcium-entry activators YC-170, CGP 28392, and BAY K 8644.

Recently, the novel dihydropyridine derivates YC-170, CGP 28392, and BAY K 8644 have been reported to act in the opposite way to Ca2+-entry blockers. We have found that these compounds inhibit the binding of [3H]nitrendipine on guinea pig heart membranes (Ki: 6 nM BAY K 8644, 115 nM CGP 28392 and 690 nM YC-170). Like those of nifedipine (Ki 1 nM), the curves had slopes close to unity, and, unlike those of some nondihydropryridine Ca2+ antagonists, were not altered in the presence of diltiazem, indicating a competitive interaction at dihydropyridine-sensitive sites. In isolated guinea pig atria, these agents exerted positively inotropic effects similar in their potency ratio to those observed in the binding experiments (BAY K 8644 1, CGP 28392 1:17, YC-170 1:600). The maximum inotropic effects of BAY K 8644 and CGP 28392, and of YC-170 corresponded respectively to two-thirds and one-third of those induced by isoprenaline or extracellular Ca2+. In the isolated rat mesenteric artery, perfused with a depolarizing solution, vasoconstrictor Ca2+ dose-response curves are shifted to the right by nifedipine. By contrast, BAY K 8644 and CGP 28392 caused a distinct leftward shift of the Ca2+ dose-response curves, at concentrations of 3-300 nM and 30-300 nM, respectively, and YC-170 a marginal shift at concentrations of 200-2000 nM, i.e., similar ranges to their inhibitory effects on [3H]nitrendipine binding. At higher concentrations, all three compounds produced Ca2+-antagonistic effects. These results indicate that the compounds act at dihydropyridine-sensitive sites and exert partial agonistic activities in vascular and myocardial tissue.[1]


  1. In vitro comparative studies of the calcium-entry activators YC-170, CGP 28392, and BAY K 8644. Rogg, H., Criscione, L., Truog, A., Meier, M. J. Cardiovasc. Pharmacol. (1985) [Pubmed]
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