Abstract
SECRETION by platelets is stimulated by agents of diverse structure such as thrombin, collagen and adrenaline; the substances secreted include adenine nucleotides, 5-hydroxytryptamine and calcium1. In many cells secretion seems to be mediated by the influx of Ca2+ (ref. 2), but this mechanism has not been demonstrated for all secretory systems and, in fact, no extracellular calcium is required for secretion by platelets. From kinetic studies of thrombin-stimulated secretion of ATP and calcium3,4 we proposed that stimulus-secretion coupling in platelets is mediated by intra-cellular calcium. We have now tested this hypothesis with the divalent cation ionophores X-537A (Lasalocid, Hoffman-La-Roche) and A23187 (Lilly). These antibiotics increase the permeability of membranes to divalent cations and can perturb intracellular cation gradients5–10. The probable mechanism involves formation of lipophilic chelate compounds10. If secretion by platelets were mediated by the intracellular release of stored calcium (or some other divalent cation) the ionophores should disrupt the intracellular ion gradients and trigger secretion. This was the observed result.
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