Calmodulin-sensitive ATP-dependent calcium transport by the rat parotid endoplasmic reticulum

Abstract

The Ca2+-dependent regulatory protein calmodulin has been shown to activate a variety of Ca2+ transport systems. We suggest here that it plays a similar regulatory function in controlling Ca2+ uptake by the endoplasmic reticulum of rat parotid glands. Like most calmodulin-sensitive systems, Ca2+ uptake by the parotid endoplasmic reticulum was inhibited by trifluoperazine. The sensitivity to inhibition was comparable to that shown by beef heart cyclic AMP phosphodiesterase activated with calmodulin. Thus, it is likely that the inhibition of Ca2+ uptake arises from specific antagonism of calmodulin function rather than other non-specific effects of the phenothiazine.