AJP - Cell Physiology, Vol 259, Issue 2 C340-C348, Copyright © 1990 by American Physiological Society
Muscarinic regulation of potassium transport in a human submandibular epithelial cell line
J. A. Ship, L. L. Patton and R. B. Wellner
Clinical Investigation and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
Results of previous studies suggest that the transport of K+ by salivary
ducts is under muscarinic control. The mechanisms by which this regulation
occurs have not been well defined, however. In this paper, we describe
mechanisms involved in the muscarinic regulation of K+ (86Rb) transport in
HSG-PA, an epithelial cell line derived from human submandibular gland
duct. Stimulation of HSG-PA cells by carbachol, a muscarinic agonist,
increases both 86Rb influx and efflux, which results in a decrease in the
equilibrium content of 86Rb within the cells. Increases in both fluxes are
dose dependent with respect to carbachol concentration, and both responses
can be blocked by atropine, a muscarinic antagonist. The
carbachol-stimulated 86Rb fluxes appear to be calcium dependent since 1)
the calcium ionophore A23187 increases 86Rb fluxes in these cells, 2) cells
loaded with 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid
(BAPTA; a calcium chelator) exhibit a reduced ability to respond to
carbachol stimulation, and 3) removal of extracellular calcium
concentration reduces the carbachol-stimulated effects. Treatment of HSG-PA
cells with 10(-7) M phorbol myristate acetate (PMA) partially blocks the
carbachol-stimulated changes in 86Rb fluxes, suggesting that protein kinase
C plays a role in this response. PMA also partially blocks
A23187-stimulated 86Rb influx, suggesting that activation of protein kinase
C inhibits muscarinic-stimulated K+ influx by blocking either the Ca2+
signal (X. He, X. Wu, and B.J. Baum. Biochem. Biophys. Res. Commun. 152:
1062-1069, 1988), steps subsequent to this effect, or both.(ABSTRACT
TRUNCATED AT 250 WORDS)
