Abstract
Bovine adrenal medulla responds to nicotinic stimulation by secreting catecholamines, but simultaneous activation of muscarinic receptors in the perfused gland depresses secretion (10). The calcium influx required for secretion is caused by nicotinic activation (3) but the breakdown of inositol phospholipids considered by Michell (8) to be responsible for mobilization of calcium is produced by muscarinic drugs only. This inositol phospholipid (phosphoinositide) effect was previously thought to be initiated by hydrolysis of phosphatidylinositol but recent work suggests that triphosphoinositide (PtdIns 4,5P2, Fig. 1), a more labile compound associated with plasma membranes and some secretory granules, is the lipid first involved (reviewed in reference 4). A possible sequence of reactions is given in Figure 2.
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© 1986 Plenum Press, New York
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Hawthorne, J.N., Swilem, AM.F. (1986). Polyphosphoinositide and Phosphoprotein Responses to Muscarinic Receptor Activation in Bovine Adrenal Medulla. In: Hanin, I. (eds) Dynamics of Cholinergic Function. Advances in Behavioral Biology, vol 30. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5194-8_92
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DOI: https://doi.org/10.1007/978-1-4684-5194-8_92
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