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<br />426
<br />
<br />JAMES E. DEACON AND W. L MINCKLEY
<br />
<br />able systems may be gleaned from reviews by Kinne (1963) and Love.
<br />(1970) and from those presented in volumes edited by Brown (1957) and
<br />Hoar and Randall (1969). Nearly all fishes investigated show initial ten-
<br />dencies to desiccate when exposed to hypersaline waters. Adjustment is
<br />accomplished by drinking water, about 70-80% of which is absorbed
<br />through the gut wall along with the monovalent ions of sodium, potassium,
<br />and chloride. The divalent ions, calcium, magnesium, and sulfate, except for
<br />small amounts that are absorbed, form insoluble oxides and hydroxid~s
<br />in the alkaline i~testinal environment and are largely eliminated via mucus
<br />tubes and with the feces. Insoluble mixed carbonate salts also left in the
<br />intestinal lumen are eventually voided., The fraction of divalent ions ab-
<br />sorbed are finally excreted by the kidney. Monovalent ions are eliminated
<br />through specialized secretory cells of the gills and sometimes in the oral
<br />epithelium, as has been demonstrated in Fundulus heteroclitus.
<br />It is of particular interest that almost all species for which data are avail-
<br />able continue to produce a urine hypotonic to their blood, even in the
<br />most hypertonic environments to which they have been experimentally sub-
<br />jected. Total urine volume, however, is greatly diminished. The one docu-
<br />mented exception is the Plains killifish (Fundulus kansae) which not only
<br />produces greatly reduced quantities of urine, but also a hypertonic urine
<br />when first introduced into hypertonic environments Temperature may
<br />greatly influence survival, since Fundulus parvipinnis desiccates in its natu-
<br />ral medium, seawater, when environmental temperatures are low. (Dou-
<br />doroff, 1945). As with virtually all other mechanisms discussed here, there
<br />are practically no data from fishes able to withstand the most extreme
<br />salinities and abrupt salinity changes of desert waters.
<br />The absence of parathyroid glands, and presumably therefore of para-
<br />thormone, appears to explain the well-known dependence of fishes on
<br />calcium in the environment. Since parathormone mobilizes calcium reserves
<br />from bones of terrestrial vertebrates, its absence in bony fishes suggests
<br />that such a mechanism does not exist. They therefore appear dependent
<br />upon environmental reserves to maintain desirable levels of the element.
<br />Marine fishes live in an environment rich in calcium, and when trans-
<br />ferred to fresh water they may suffer numerous complications or even
<br />death due to a complex of responses centering around a calcium
<br />deficiency caused by a general increase in membrane permeability. The
<br />antagonistic mechanism, i.e., control of hypercalcemia, involves production
<br />of calcitonin by the unusually well-developed ultimobranchial bodies of
<br />gnathostome fishcs. The probable function of calcitonin is control of calcium
<br />transport across ccll mcmbranes, especially in the gut, kidney, and/or gill
<br />surfaces. Additional evidence has bcen prescnted to suggest that calcitonin
<br />may function in suppressing calcium resorption from bone in fishes with
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