Phosphoinositide breakdown in isolated rat parotid membranes. Stimulation by cholinergic and alpha-adrenergic agonists.
Parotid gland membranes labelled with [3H]inositol were challenged with the cholinergic agonist, carbamylcholine, or with epinephrine in the presence of propranolol. Both agonists caused a significant breakdown of labelled phosphoinositides (17.5%) in membranes suspended in Krebs-Ringer bicarbonate buffer. This effect was abolished by the respective antagonists, atropine or phentolamine. The carbamylcholine-induced breakdown of labelled phosphoinositides did not require cytosol. The addition of cytosol alone, or the exposure of membranes to a medium of low ionic strength caused a significant breakdown of phosphoinositides (10-40%). No further breakdown due to the addition of carbamylcholine was observed under these conditions. It is suggested that neurotransmitter-induced breakdown of phosphoinositides is effected by membrane-associated enzyme(s) and can be observed only in a medium of high ionic strength.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002021:Buffers; D002217:Carbachol / Q000494:pharmacology*; D002462:Cell Membrane / Q000378:metabolism; D003600:Cytosol / Q000502:physiology; D004837:Epinephrine / Q000494:pharmacology*; D007294:Inositol / Q000378:metabolism; D009994:Osmolar Concentration; D010306:Parotid Gland / Q000187:drug effects / Q000378:metabolism*; D010716:Phosphatidylinositols / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats
D002021:Buffers; D010716:Phosphatidylinositols; D007294:Inositol; D001285:Atropine; D002217:Carbachol; D011433:Propranolol; D004837:Epinephrine