Abstract
THE release of neurohypophyseal hormones, whether evoked by electrical stimulation or by a high potassium concentration, is associated with an uptake of calcium from the extracellular space1–4. It has therefore been proposed that calcium entry plays a key role in stimulus-secretion coupling in the neurohypophysis5–7. Recently, calcium ionophores have been described which increase calcium flux across the cell membrane and induce secretion in a number of secretory systems8–12. In contrast, we report that although the calcium ionophore X-537A (Lasalocid, Hofmann-LaRoche) promotes secretion from the rat neurohypophysis, there is no corresponding increase in calcium uptake; furthermore, ionophore-induced secretion persists in the absence of external calcium ions. The most logical explanation for these results is that, rather than increasing the influx of extra-cellular calcium, the ionophore actually releases calcium from intracellular binding sites, probably mitochondria; and that it is the mobilisation of this internal calcium which, inter alia, promotes secretion.
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NORDMANN, J., CURRELL, G. The mechanism of calcium ionophore-induced secretion from the rat neurohypophysis. Nature 253, 646–647 (1975). https://doi.org/10.1038/253646a0
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DOI: https://doi.org/10.1038/253646a0
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