Abstract

AbstractThis article attempts to review mechanisms of intra‐ (ICF) and extracellular fluid (ECF) acid‐base balance and the contribution each makes to whole animal acid‐base homeostasis in an evolutionary progression of crustaceans (marine, freshwater, semi‐ and fully terrestrial). ICF pH (pHi) is regulated to preserve the functional integrity of enzymes involved in cell metabolism. The ECF is the intermediary between cellular acid/base production and whole animal exchange at the primary epithelia, the gills, and antennal gland. In vivo regulation of pHi is discussed under selected environmental conditions. Compensatory mechanisms include intracellular buffering and transmembrane exchange of acidic/base equivalents including primarily an Na + /H + /HCO3 −/Cl− mechanism and an Na + /H + exchanger. Acid‐base values and regulation in the ECF (which may be subcompartmented in selected tissues) differ in aquatic versus terrestrial species. The latter have higher PCO2 (and lower pH) associated with reduced ventilation due to the higher O2 capacitance of air. Correspondingly they can regulate ECF pH (pHe) by respiratory control of PCO2; terrestrial species also depend upon mobilization of exoskeletal CaCO3 to buffer protons. In aquatic species the primary mechanism of acid‐base regulation is via electroneutral ion exchangers (Na +/acidic equivalent; Cl −/basic equivalent) primarily at the branchial epithelium but also apparent in the renal tubule in species that produce dilute urine (hyperosmo/ionoregulators). Evidence is presented for dynamic regulation of unidirectional branchial and renal ion fluxes for purposes of acid‐base regulation. Quantitatively the antennal gland typically contributes only 10% of the overall response. Stoichiometrically, whole animal acidic/basic equivalents exchanged at these epithelia originate predominantly in the ICF compartment (50‐‐95%). Future perspectives emphasize the need to better understand how pH compensation or in some cases tolerance is related to cellular function. © 1992 Wiley‐Liss, Inc.

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