{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T11:08:59Z","timestamp":1761217739261},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1985,11,1]],"date-time":"1985-11-01T00:00:00Z","timestamp":499651200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1985,11]]},"abstract":"<jats:p>ADP produces a rapid elevation in the concentration of cytoplasmic free calcium, [Ca2+]i, in quin2\u2010loaded human platelets which begins within 1 s of stimulation and peaks after 10 s. In the presence of 1 mM\u2010extracellular calcium, [Ca2+]i peaks at 670 +\/\u2010 50 nM in the absence and 610 +\/\u2010 30 nM in the presence of a cyclo\u2010oxygenase inhibitor. The production of prostaglandin endoperoxides and thromboxane A2 are not required for stimulation of Ca2+ fluxes by ADP but appear to have a supportive role. In the absence of extracellular calcium ions and with 1 mM\u2010extracellular EGTA, stimulation with ADP caused [Ca2+]i to peak at 160 +\/\u2010 20 nM in the absence and 150 +\/\u2010 10 nM in the presence of a cyclo\u2010oxygenase inhibitor. ADP can cause the discharge of calcium ions from internal stores and does not require the prior formation of prostaglandin endoperoxides or thromboxane A2. The rise in [Ca2+]i in the presence of extracellular Ca2+ is sixfold larger than in the absence of extracellular Ca2+. This suggests that the major component of the ADP\u2010stimulated rise in [Ca2+]i is caused by the influx of Ca2+ ions across the plasma membrane. Diltiazem, D600, nimodipine and nifedipine had little or no effect on resting or ADP\u2010stimulated [Ca2+]i levels. Depolarization with potassium\u2010rich media alone or in conjunction with valinomycin had no effect on basal [Ca2+]i and only a partial inhibitory effect on ADP\u2010stimulated increases in [Ca2+]i. Depolarization had no effect on the ADP\u2010stimulated rise in [Ca2+]i in Ca2+\u2010free media. Hyperpolarization had no marked effect on the rise in [Ca2+]i produced by ADP in the presence of extracellular calcium. These results are consistent with there being no voltage\u2010dependent channels in the platelet plasma membrane. Using ionomycin, a selective Ca2+ ionophore, and measuring both quin2 fluorescence and optical density of the suspension simultaneously, the threshold [Ca2+]i for shape change was determined to be 300 nM with half\u2010maximal effect at 500 nM and maximal shape change at 800 nM. ADP produced maximal shape change confirmed by scanning electron microscopy with corresponding [Ca2+]i at below 200 nM. The level of [Ca2+]i required to produce aggregation using ionomycin was approximately 1 microM. ADP alone, or following a smaller rise in [Ca2+]i produced by ionomycin to disguise the effect of ADP, produced an aggregatory response at concentrations below 1 microM. These data indicate that excitatory mechanisms are involved producing shape change and aggregation to ADP other than a stimulated rise in [Ca2+]i.<\/jats:p>","DOI":"10.1113\/jphysiol.1985.sp015850","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T06:45:37Z","timestamp":1418971537000},"page":"131-146","source":"Crossref","is-referenced-by-count":101,"title":["Responses to adenosine diphosphate in human platelets loaded with the fluorescent calcium indicator quin2."],"prefix":"10.1113","volume":"368","author":[{"given":"T J","family":"Hallam","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T J","family":"Rink","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1985,11]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1985.sp015850","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1985.sp015850","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,21]],"date-time":"2023-10-21T15:50:15Z","timestamp":1697903415000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1985.sp015850"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1985,11]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1985,11]]}},"alternative-id":["10.1113\/jphysiol.1985.sp015850"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1985.sp015850","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1985,11]]}}}