Abstract
The effects of depolarizing conditions resulting from increasing extracellular K+ concentration or nystatin treatment on intracellular Ca2+ concentration ([Ca2+]i) were studied in guinea pig antral mucous cells following acetylcholine (ACh) stimulation. ACh stimulation evoked a biphasic increase in [Ca2+]i, that is, an initial transient increase followed by a plateau. Depolarizing conditions reduced the [Ca2+]i in the plateau phase during ACh stimulation. However, pertussis toxin (PTX, a G protein inhibitor) treatment caused [Ca2+]i in the ACh-evoked plateau phase to increase under depolarizing conditions, while it had no effect on [Ca2+]i under hyperpolarized conditions. Based on these observations, Ca2+ permeable channels are regulated by a G protein which is activated by depolarized conditions and inhibited by hyperpolarized conditions and PTX; activation of the G protein (depolarization) causes Ca2+ permeable channels to inhibit, and in turn, inhibition of the G protein (hyperpolarization) causes them to activate.
