{"refrec":{"BRefID":285087,"RR":"<b>Lindinger, M.I.; Lauren, D.J.; McDonald, D.G.</b> (1984). Acid-base balance in the sea mussel, <i>Mytilus edulis</i>. III. Effects of environmental hypercapnia on intra- and extracellular acid–base balance. <i>Mar. Biol. Lett. 5(6)</i>: 371-381","BEntID":277112,"PublicFlag":1,"CheckedFlag":0,"wosflag":0,"vabbflag":null,"RefStringPartII":". <i>Mar. Biol. Lett. 5(6)</i>: 371-381","DocTypID":8,"DocType":"Journal article","MarineFlag":1,"FreshFlag":0,"BrackishFlag":0,"TerrestrialFlag":0,"Authorstring":"Lindinger, M.I.; Lauren, D.J.; McDonald, D.G.","OrigTitleTranslFlag":0,"Authorstringtrunc":"Lindinger, M.I. <i>et al.</i>","Englishabstract":"Exposure of M. edulis L. to normoxic-hypercapnic seawater (PCO2 = 6.5, 13.0, and 26.0 mm Hg) for 24 h produced an elevation in hemolymph [H+], [Ca2+], [HCO3-], [HN4-], and PCO2. Simultaneous measurement of intracellular pH (pHi) at a PCO2 of 26 mm Hg showed that pHi followed hemolymph pH but was maintained about 0.4 pH unit lower. A large (6.37 .+-. 0.65 meq. H+/L) nonrespiratory component to the intracellular acidosis developed within 0.5 h of exposure to PCO2 of 26 mmHg. At all CO2 levels, the initial drop in pH was partially compensated over the remaining 23.5 h of CO2 exposure by increases in extracellular and intracellular bicarbonate, while PCO2 remained constant. About 70-80% of the additional bicarbonate was produced by the dissolution of shell and body fluid stores of CaCO3; the remainder may have resulted from intracellular to extracellular ion exchanges and/or transepithelial ion exchange processes. Acid-base regulation in M. edulis is largely passive in response to environmental hypercapnia. 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