Influence of glycosylation inhibitors on dihydropyridine binding to cardiac cells.

Abstract

In primary cultures of neonatal rat heart cells we found a linear correlation between the number of L-type calcium channel-specific dihydropyridine (DHP) binding sites and spontaneous beating frequency (v). Formation of glycoproteins in tissue culture was suppressed by different inhibitors of N-glycosylation. This inhibition alters to a different extent the binding of the DHP ligand (+)-[methyl-3H]PN 200-110 and v. The most severe but reversible effect occurs at 6 micrograms/ml tunicamycin (Bmax approximately 45% and v approximately 6%, resp., of control), a slight increase in Bmax at 0.1-0.5 mM castanospermine and 0.05-2.5 mM deoxymannojirimycin. The other inhibitors gave no significant alteration of Bmax.