Lanthanum as a Tool to Study the Role of Phosphatidylinositol in the Calcium Transport in Rat Parotid Glands upon Cholinergic Stimulation

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Abstract
The effects of La on protein secretion, K+ efflux, Ca uptake and phosphatidylinositol turnover stimulated by cholinergic agonists in rat parotid glands was described. Carbachol increases in vitro Ca uptake, protein secretion and K+ efflux through muscarinic receptor; however it fails to stimulate protein discharge or K+ release in an incubation medium free of calcium. La inhibits Ca uptake, protein secretion and K+ efflux induced by carbachol without impairing protein discharge stimulated by norepinephrine through the .beta.-adrenergic receptor. Norepinephrine, in the presence of Ca in the incubation medium, stimulates the K+ efflux through the .alpha.-adrenergic receptor: this effect is suppressed by La. These results emphasize the role of increased influx of Ca in the cellular phenomena controlled by muscarinic or .alpha.-adrenergic receptors. Carbachol increases phosphatidylinositol turnover in the absence of Ca in extracellular medium; carbachol increases the rate of phosphatidylinositol breakdown and that La impairs this cholinergic effect. The interaction between cholinergic agonist and muscarinic receptor could induce a stimulation of phosphatidylinositol turnover which could control the Ca influx according to the gradient through the plasmalemma membrane.