Abstract

Changes in phosphoinositide metabolism due to muscarinic stimulation of the adrenal medulla are reviewed. Evidence is presented that muscarinic receptors inhibit catecholamine secretion by the bovine gland and that muscarinic agonists do not cause entry of calcium ions. Results are inconsistent with the theory that phosphatidylinositol hydrolysis opens calcium ‘gates’. Polyphosphoinositide metabolism is also reviewed and the suggestion made that phosphatidylinositol 4,5-bisphosphate may regulate the activity of the calcium pump ATPase in cells where phosphoinositide-linked receptors promote calcium influx.

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