We explored the relationship between nucleotide-evoked changes in intracellular free calcium ([Ca2+] i ) and anion secretion by measuring [Ca2+] i and I SC simultaneously in Fura-2-loaded, cultured equine sweat gland epithelia. Apical ATP, UTP or UDP elicited sustained increases in [Ca2+] i that were initiated by the mobilization of cytoplasmic Ca2+ but maintained by Ca2+ influx. However, although these nucleotides also increased I SC , this response was transient whereas the [Ca2+] i signals were sustained. Experiments in which external Ca2+ was removed/replaced showed that Ca2+ entering nucleotide-stimulated cells elicited very little change in I SC . Cross desensitization experiments showed that UTP-stimulated epithelia became insensitive to ATP but that UTP could increase both [Ca2+] i and I SC in ATP-stimulated cells by activating `pyrimidinoceptors' essentially insensitive to ATP. Thapsigargin evoked a sustained rise in [Ca2+] i that was accompanied by a maintained increase in I SC . However, this increase in I SC was dependent upon external Ca2+ and so the responses to nucleotides and thapsigargin have different properties. ATP increased I SC in thapsigargin-treated cells without causing any rise in [Ca2+] i while ionomycin increased both parameters. The data therefore show that apical P2Y receptors allow nucleotides to increase I SC via two mechanisms, one of which appears to be [Ca2+] i -independent control of anion channels.
The Journal of Membrane Biology – Springer Journals
Published: Aug 1, 1999
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