{"title":"胰腺b细胞刺激-分泌偶联的数学模型II。钙刺激钙释放","authors":"Y. Scholler, V. de Maertelaer, W.J. Malaisse","doi":"10.1016/0010-468X(85)90002-9","DOIUrl":null,"url":null,"abstract":"<div><p>An attempt was made to simulate in a mathematical model one of the two major effects of glucose upon <sup>45</sup>Ca fractional outflow rate from prelabelled pancreatic islets, namely the increase in effluent radioactivity which is currently ascribed to the displacement of <sup>45</sup>Ca from intracellular sites, as resulting from a facilitated influx of unlabelled <sup>40</sup>Ca into the islet cells. The occurrence of such a rise in effluent radioactivity and its suppression in the absence of extracellular Ca<sup>2+</sup> could only be simulated if the release of Ca by the vacuolar system was assumed to be stimulated by a rise in the cytosolic Ca concentration. It is proposed therefore that, in islets like in muscle, a process of Ca-stimulated Ca release may participate in the regulation of intracellular Ca distribution.</p></div>","PeriodicalId":75731,"journal":{"name":"Computer programs in biomedicine","volume":"19 2","pages":"Pages 119-126"},"PeriodicalIF":0.0000,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0010-468X(85)90002-9","citationCount":"7","resultStr":"{\"title\":\"Mathematical modelling of stimulus-secretion coupling in the pancreatic B-cell II. Calcium-stimulated calcium release\",\"authors\":\"Y. Scholler, V. de Maertelaer, W.J. Malaisse\",\"doi\":\"10.1016/0010-468X(85)90002-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>An attempt was made to simulate in a mathematical model one of the two major effects of glucose upon <sup>45</sup>Ca fractional outflow rate from prelabelled pancreatic islets, namely the increase in effluent radioactivity which is currently ascribed to the displacement of <sup>45</sup>Ca from intracellular sites, as resulting from a facilitated influx of unlabelled <sup>40</sup>Ca into the islet cells. The occurrence of such a rise in effluent radioactivity and its suppression in the absence of extracellular Ca<sup>2+</sup> could only be simulated if the release of Ca by the vacuolar system was assumed to be stimulated by a rise in the cytosolic Ca concentration. It is proposed therefore that, in islets like in muscle, a process of Ca-stimulated Ca release may participate in the regulation of intracellular Ca distribution.</p></div>\",\"PeriodicalId\":75731,\"journal\":{\"name\":\"Computer programs in biomedicine\",\"volume\":\"19 2\",\"pages\":\"Pages 119-126\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1985-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0010-468X(85)90002-9\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Computer programs in biomedicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0010468X85900029\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Computer programs in biomedicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0010468X85900029","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Mathematical modelling of stimulus-secretion coupling in the pancreatic B-cell II. Calcium-stimulated calcium release
An attempt was made to simulate in a mathematical model one of the two major effects of glucose upon 45Ca fractional outflow rate from prelabelled pancreatic islets, namely the increase in effluent radioactivity which is currently ascribed to the displacement of 45Ca from intracellular sites, as resulting from a facilitated influx of unlabelled 40Ca into the islet cells. The occurrence of such a rise in effluent radioactivity and its suppression in the absence of extracellular Ca2+ could only be simulated if the release of Ca by the vacuolar system was assumed to be stimulated by a rise in the cytosolic Ca concentration. It is proposed therefore that, in islets like in muscle, a process of Ca-stimulated Ca release may participate in the regulation of intracellular Ca distribution.