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THE positive inotropic effect of digitalis compounds is generally attributed to an increase in the amount of activator calcium1 and not to a change in the calcium sensitivity of regulatory contractile proteins2,3. The main question is the cellular or subcellular basis of the increase in the myoplasmic calcium transient. Since calcium entry through the slow inward current may play an important part in excitation–contraction coupling, it has been suggested that the slow inward current might be enhanced by digitalis4,5. All the evidence has been negative6–11 apart from a report by Dramane et al.12 and results of H. Brown, W. Giles and S. Noble (personal communication). We have re-examined this question and have found that strophanthidin can increase the slow inward current and alter its re-priming kinetics in certain conditions. These observations may provide a partial explanation of the positive inotropic effect observed in the same experiments.

CELLS incubated in an amino acid-free Krebs–Ringer buffer, or grown in medium with a reduced amino acid concentration, respond by increasing their ability to actively transport amino acids1–3. Studies using inhibitors of mRNA transcription and translocation suggested that this regulatory control involves mRNA transcription and the synthesis of protein intimately concerned with the transport process. We determined nuclear involvement using cells enucleated by prior treatment with the fungal metabolite cytochalasin B (ref. 4). The results presented here suggest that the nuclei of HeLa cells are important for maintaining and modifying their amino acid transport capacity in response to a reduction in the external amino acid concentration.