Abstract
The metabolism of phosphatidylinositol and phosphatidate was investigated in fragments of longitudinal smooth muscle from guinea pig ileum incubated with cholinergic and anticholinergic drugs. Incorporation of P(i) into these lipids was enhanced by acetylcholine and carbamoylcholine. The receptor responsible for triggering this response was of the muscarinic type, since the response was also produced by the muscarinic agonists acetyl β methylcholine, carbamoyl β methylcholine and pilocarpine, and the response was prevented by atropine and propylbenzilylcholine mustard, but not by tubocurarine. Increased phosphatidylinositol labelling was clearly observed within 5 min in tissue treated with a high concentration of carbamoylcholine. Half maximal stimulation of phosphatidylinositol labelling occurred at approx. 10μM carbamoylcholine. Incubation of muscle fragments with carbamoylcholine provoked a decrease in phospatidylinositol concentration, as would be expected if phosphatidylinositol breakdown is the reaction controlled by agonists. This information all appears consistent with the proposal that phosphatidylinositol breakdown may be a reaction intrinsic to the mechanisms of muscarinic cholinergic receptor systems.
Original language | English |
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Pages (from-to) | 653-657 |
Number of pages | 5 |
Journal | Biochemical Journal |
Volume | 154 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 Jan 1976 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology