Abstract
NORADRENALINE produces increased uptake of 32Pi into acidic phospholipids in the nervous system1–4, and neurotransmitters and other stimuli do so in various tissues5–7. The rat pineal gland responds to noradrenaline in similar fashion8–10. We have shown already that the mechanism by which noradrenaline stimulates phospholipid metabolism in the pineal gland does not depend on protein synthesis and does not involve either β-adrenergic receptors or cyclic AMP10. We also observed that the β-adrenergic receptor blocking agent propranolol not only failed to counteract the influence of noradrenaline, but itself markedly enhanced the incorporation of 32Pi into phospholipids to give a labelling pattern distinct from that produced by noradrenaline10,11. We concluded that this action of propranolol was due to its local anaesthetic or membrane perturbing property, since sotalol, a β-adrenergic receptor blocking agent without these other effects12, had no influence on phospholipid metabolism. In addition, a series of local anaesthetics yield effects comparable with those of propranolol13.
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HAUSER, G., SHEIN, H. & EICHBERG, J. Relationship of α-adrenergic receptors in rat pineal gland to drug-induced stimulation of phospholipid metabolism. Nature 252, 482–483 (1974). https://doi.org/10.1038/252482a0
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DOI: https://doi.org/10.1038/252482a0
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