Abstract
Semicarbazide hydrochloride and isonicotinic acid hydrazide, which are both inhibitors of phosphopyridoxal-dependent systems, inhibit the increase in the rate of beating of hearts which is brought about by breis of corpora cardiaca. This inhibition is partially reversed by phosphopyridoxal. Semicarbazide decreases the percentage of argentaffin-positive cells among pericardial cells exposed to breis of corpora cardiaca. DOPA increases the rate of beating of the isolated heart. This increase is mediated by the pericardial cells and is inhibited by semicarbazide. The inhibition by semicarbazide is reversed by phosphopyridoxal. It is suggested, as a working hypothesis, that the hormone from the corpus cardiacum stimulates the pericardial cells to produce an amine from an amino acid by the action of the appropriate amino acid decarboxylase. The hormone intervenes either by causing the cells to produce more of the amino acid, or by unmasking the amino acid which is pictured as being protected from the enzyme in the unstimulated cell.