Maximally effective concentrations of dibutyryl 3’,5’-AMP (dbcAMP), aminophylline, D- and DL-propranolol (PROP), parathyroid extract (PTE) and parathyroid hormone (PTH) result in a 30–80% stimulation of the aerobic lactate production in embryonic mouse calvarium explants. Optimal doses of dbcAMP, aminophylline, D- and DL-PROP when combined with a suboptimal concentration of PTE are either not fully additive or even inhibitory to the action of PTE on bone glycolysis. dbcAMP (0.S0 HIM) induces bone demineralization (Ca and P1 release) but compared with PTE, the effect is small and occurs only after an extended period of cultivation (48 hr). A lower dbcAMP concentration (0.13 HIM), however, causes a small but significant increase in the Ca release after 24 hr of cultivation. Under those circumstances the P1 release also increases, although not significantly. Aminophylline (1.25 HIM), D- (0.10 mil), and DL-PROP (0.10 DIM) significantly increase the uptake of Ca and P1 from the medium, whereas the addition of dbcAMP (0.13–1.0 mM), aminophylline (0.50–1.0 nffl), D- (0.04 mM) or DL-PROP (0.04 mM) strongly inhibit PTH-induced bone demineralization. The results of our studies are interpreted as evidence that (1) Cyclic AMP is not the exclusive mediator in the action of PTH on bone resorption. (2) Aminophylline and dbcAMP, in addition to their well-known inhibitory effect on bone phosphodiesterase activity, presumably also act by raising the cytoplasmic Ca concentration, thereby influencing the PTE-stimulated Ca transport mechanism. (3) When affecting PTE-induced bone resorption, PROP is suggested to act as a membrane stabilizer and not by a mechanism involving β-receptor blockade. (Endocrinology94: 424, 1974))