Abstract
The effects of receptor stimulation on net fluxes of 45Ca in parotid acinar cells were investigated. When cellular 45Ca content was near steady-state, muscarinic receptor activation by carbachol caused a net efflux of 45Ca (not always reproducible) followed by a net influx. In the presence of excess ethylene glycol bis (beta-aminoethyl ether) N,N,N,N-tetraacetic acid, net efflux invariably occurred, but the influx phase was prevented. When the muscarinic receptor antagonist atropine was added to the medium during the influx phase, an abrupt transient influx occurred followed by a return of net influx to the prestimulation level. When cellular responses believed to reflect intracellular ionized Ca (k + permeability, protein secretion) were examined under similar conditions, atropine invariably had an inhibitory effect. The Ca taken up in response to atropine apparently replenishes the hormone-sensitive pool of cellular Ca since it can be released subsequently by adrenoceptor activation. Taken together, these observations suggest that when atropine is administered to cholinergically activated cells, the hormone-sensitive Ca pool rapidly refills from the extracellular fluid without a concomitant increase in ionized intracellular Ca. Thus, it is suggested that this Ca pool is most likely associated with the plasma membrane.
MeSH Terms
Animals
Atropine/pharmacology
Biological Transport/drug effects
Calcium/metabolism
Carbachol/pharmacology
Cell Membrane/drug effects,metabolism
Egtazic Acid/pharmacology
In Vitro Techniques
Kinetics
Male
Parotid Gland/drug effects,metabolism
Rats
Rats, Inbred Strains
Receptors, Cholinergic/drug effects
Receptors, Muscarinic/drug effects
Chemicals
Receptors, Cholinergic
Receptors, Muscarinic
Egtazic Acid
Atropine
Carbachol
Calcium
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Poggioli J
Putney J W
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19 references, click to expand
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