scholarly journals Cholinergically stimulated phosphatidylinositol breakdown in parotid-gland fragments is independent of the ionic environment

1976 ◽  
Vol 158 (2) ◽  
pp. 505-507 ◽  
Author(s):  
L M Jones ◽  
R H Michell
Keyword(s):  
Parotid Gland ◽  
Cyclic Nucleotides ◽  
Direct Interaction ◽  
Cholinergic Receptor ◽  
Receptor System ◽  
Muscarinic Cholinergic Receptor ◽  
Rat Parotid Gland ◽  
Sucrose Medium ◽  
Muscarinic Cholinergic ◽  
Rat Parotid

Carbamoylcholine stimulated phosphatidylinositol breakdown in rat parotid-gland fragments incubated in either a Krebs--Ringer medium or an ion-depleted iso-osmotic sucrose medium. This suggest that phosphatidylinositol breakdown is not initiated by a change in the intracellular concentration of Na+ or of K+, and previous experiments have already indicated that it is independent of cyclic nucleotides and Ca2+. Thus it seems that this reaction may be initiated by a direct interaction at the plasma membrane between the activated muscarinic cholinergic receptor system and the enzyme that catalyses phosphatidylinositol breakdown.

scholarly journals The relationship of calcium to receptor-controlled stimulation of phosphatidylinositol turnover. Effects of acetylcholine, adrenaline, calcium ions, cinchocaine and a bivalent cation ionophore on rat parotid-gland fragments

1975 ◽  
Vol 148 (3) ◽  
pp. 479-485 ◽  
Author(s):  
L M Jones ◽  
R H Michell
Keyword(s):  
Parotid Gland ◽  
De Novo ◽  
Head Group ◽  
Ionophore A23187 ◽  
Bivalent Cation ◽  
Phosphatidylinositol Turnover ◽  
Rat Parotid Gland ◽  
Muscarinic Cholinergic ◽  
Rat Parotid ◽  
Stimulation Of

The possibility that Ca2+ ions are involved in the control of the increased phosphatidylinositol turnover which is provoked by alpha-adrenergic or muscarinic cholinergic stimulation of rat parotid-gland fragments has been investigated. Both types of stimulation provoked phosphatidylinositol breakdown, which was detected either chemically or radiochemically, and provoked a compensatory synthesis of the lipid, detected as an increased rate of incorporation of 32Pi into phosphatidylinositol. Acetylcholine had little effect on the incorporation of labelled glycerol, whereas adrenaline stimulated it significantly, but to a much lower extent than 32P incorporation: this suggests that the response to acetylcholine was entirely accounted for by renewal of the phosphorylinositol head-group of the lipid, but that some synthesis de novo was involved in the response to adrenaline. The responses to both types of stimulation, whether measured as phosphatidylinositol breakdown or as phosphatidylinositol labelling, occurred equally well in incubation media containing 2.5 mm-Ca2+ or 0.2 mm-EGTA [ethanedioxybis(ethylamine)-tetra-acetic acid]. Incubation with a bivalent cation ionophore (A23187) led to a small and more variable increase in phosphatidylinositol labelling with 32Pi, which occurred whether or not Ca2+ was available in the extracellular medium: this was not accompanied by significant phosphatidylinositol breakdown. Cinchocaine, a local anaesthetic, produced parallel increases in the incorporation of Pi and glycerol into phosphatidylinositol. This is compatible with its known ability to inhibit phosphatidate phosphohydrolase (EC 3.1.3.4) and increase phosphatidylinositol synthesis de novo in other cells. These results indicate that the phosphatidylinositol turnover evoked by alpha-adrenergic or muscarinic cholinergic stimuli in rat parotid gland probably does not depend on an influx of Ca2+ into the cells in response to stimulation. This is in marked contrast with the K+ efflux from this tissue, which is controlled by the same receptors, but is strictly dependent on the presence of extracellular Ca2+. The Ca2+-independence of stimulated phosphatidylinositol metabolism may mean that it is controlled through a mode of receptor function different from that which controls other cell responses. Alternatively, it can be interpreted as indicating that stimulated phosphatidylinositol breakdown is intimately involved in the mechanisms of action of alpha-adrenergic and muscarinic cholinergic receptor systems.

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