Abstract Carbachol, substance P and epinephrine, but not isoproterenol, transiently stimulated O 2 consumption by 40–50% in rat parotid gland slices. The response to carbachol, but not to substance P, was blocked by atropine. Ouabain (1 mM) did not affect the response to carbachol. Also, the response to carbachol did not require external Ca, and was not significantly diminished by 1.0 mM LaCl 3 . Reintroduction of Ca to a low Ca medium increased O 2 consumption only if carbachol was present. Procaine inhibited the increase in O 2 consumption due to carbachol, but not that due to substance P. When both carbachol and substance P were presented to the tissues in series and in the absence of external Ca, the second agonist failed to produce a response. When these results are considered in the light of previous studies on Ca and the responses of the parotid gland, they suggest that the primary stimulus for the O 2 consumption is the release of a limited pool of membrane-bound Ca following receptor activation.