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