has also been identified in the gills of the killifish (EpSTEIN et al., 1967) and Japanese, European and American eels (UTIDA et al., 1966; MOTAIS, 1970; JAMPOL and
EpSTEIN, 1970). The activity of this enzyme also increases considerably when these
fish are transferred from fresh water to sea-water. The levels of Na-K acuvated
ATPase in the gills are also 4 to 5 times greater in teleosts that normally are exclusively confined to sea-water than in those which are limited to fresh water (KAMIYA
and UTIDA, 1969 ; JAMPOL and EpSTEIN, 1970). Marine chondrichthyean fishes had
similar branchial enzyme levels to the fresh water teleosts. In other tissues, this enzyme is known to be intimately concerned with active sodium transport and a specific inhibitor of its activity, ouabain, has been shown to abolish the ability of the
isolated gills of the Japanese eel to secrete sodium (KAMIYA, 1967; KAMIYA and
UTIDA, 1968). This enzyme also requires potassium for its activation and the flounder fails to extrude sodium from its gills when potassium is excluded from the surrounding sea-water solution (MAETZ, 1969 b). It is not known whether the Na-K
activated ATPase is present in 'chloride secreting' (or 'mitochondria-rich') cells,
but the pseudobranch of the killifish is particularly rich in these cells as well as the
enzyme (EpSTEIN et al., 1967). The increased active extrusion of sodium that occurs
from the gills of eels after they are adapted to sea-water can be prevented when they
are treated with actinomycin D (MAETZ et al., 1969 b) . This antibiotic specifically
inhibits nuclear RNA polymerase and so prevents the formation of RNA and protein synthesis. The increase in the activity of Na-K ATPase is also prevented
(MOTAIS, 1970). It seems likely that the antibiotic is acting to reduce protein synthesis (including Na-K ATPase) and the increased branchial cell differentiation that
accompanies the adaptation of eels to sea-water.
When killifish are hypophysectomized the increase in activity of the branchial
Na-K activated ATPase in sea-water does not occur (EpSTEIN et al., 1967). This
effect was, however, not observed in the Japanese eel (UTIDA et al., 1966). Unequivocal evidence for a hormonal role in the increased induction of this enzyme is
thus lacking. Nevertheless, endocrines can influence the process of sodium transport across the gills in a more direct manner, but just how they interact with NaK activated ATPase is unknown. Injections of neurohypophysial peptides, vasotocin and oxytocin, facilitate the branchial outflux of sodium that occurs when the
flounder is transferred from fresh water to sea-water (MOTAIS and MAETZ, 1967).
The mechanism of this effect is not clear but it could reflect the vasoactive properties of such peptides in changing the circulation of blood in the gills (MAETZ,
1968). Corticotrophin, when injected, also increases the rate of sodium exchange
across the gills of eels in sea-water and cortisol and aldosterone have a similar effect
(MAYER and MAETZ; 1967). The mammalian adenohypophysial hormone prolactin
reduces branchial sodium exchanges in killifish, Fundulus beteroclitus, in sea-water
(MAETZ, MOTAIS, and MAYER, 1969). The physiological significance of such observations is not clear at present and will be discussed later.
~) Gills in Fresh Water. Fishes in fresh water exchange sodium with the fluid that
bathes them at less than 1% of the rate in sea-water (Table 7.9). In the goldfish
nearly all of the sodium loss is accounted for by that in the urine, while in the eel
and flounder extrarenal losses make up about 10% of the total (Tables 7.9 and 7.7).
In fish that are not feeding the accumulation of sodium is almost entirely accounted
for by the active uptake of sodium across the gills. KROGH (1939) depleted goldfish
222
EpSTEIN, 1970). The activity of this enzyme also increases considerably when these
fish are transferred from fresh water to sea-water. The levels of Na-K acuvated
ATPase in the gills are also 4 to 5 times greater in teleosts that normally are exclusively confined to sea-water than in those which are limited to fresh water (KAMIYA
and UTIDA, 1969 ; JAMPOL and EpSTEIN, 1970). Marine chondrichthyean fishes had
similar branchial enzyme levels to the fresh water teleosts. In other tissues, this enzyme is known to be intimately concerned with active sodium transport and a specific inhibitor of its activity, ouabain, has been shown to abolish the ability of the
isolated gills of the Japanese eel to secrete sodium (KAMIYA, 1967; KAMIYA and
UTIDA, 1968). This enzyme also requires potassium for its activation and the flounder fails to extrude sodium from its gills when potassium is excluded from the surrounding sea-water solution (MAETZ, 1969 b). It is not known whether the Na-K
activated ATPase is present in 'chloride secreting' (or 'mitochondria-rich') cells,
but the pseudobranch of the killifish is particularly rich in these cells as well as the
enzyme (EpSTEIN et al., 1967). The increased active extrusion of sodium that occurs
from the gills of eels after they are adapted to sea-water can be prevented when they
are treated with actinomycin D (MAETZ et al., 1969 b) . This antibiotic specifically
inhibits nuclear RNA polymerase and so prevents the formation of RNA and protein synthesis. The increase in the activity of Na-K ATPase is also prevented
(MOTAIS, 1970). It seems likely that the antibiotic is acting to reduce protein synthesis (including Na-K ATPase) and the increased branchial cell differentiation that
accompanies the adaptation of eels to sea-water.
When killifish are hypophysectomized the increase in activity of the branchial
Na-K activated ATPase in sea-water does not occur (EpSTEIN et al., 1967). This
effect was, however, not observed in the Japanese eel (UTIDA et al., 1966). Unequivocal evidence for a hormonal role in the increased induction of this enzyme is
thus lacking. Nevertheless, endocrines can influence the process of sodium transport across the gills in a more direct manner, but just how they interact with NaK activated ATPase is unknown. Injections of neurohypophysial peptides, vasotocin and oxytocin, facilitate the branchial outflux of sodium that occurs when the
flounder is transferred from fresh water to sea-water (MOTAIS and MAETZ, 1967).
The mechanism of this effect is not clear but it could reflect the vasoactive properties of such peptides in changing the circulation of blood in the gills (MAETZ,
1968). Corticotrophin, when injected, also increases the rate of sodium exchange
across the gills of eels in sea-water and cortisol and aldosterone have a similar effect
(MAYER and MAETZ; 1967). The mammalian adenohypophysial hormone prolactin
reduces branchial sodium exchanges in killifish, Fundulus beteroclitus, in sea-water
(MAETZ, MOTAIS, and MAYER, 1969). The physiological significance of such observations is not clear at present and will be discussed later.
~) Gills in Fresh Water. Fishes in fresh water exchange sodium with the fluid that
bathes them at less than 1% of the rate in sea-water (Table 7.9). In the goldfish
nearly all of the sodium loss is accounted for by that in the urine, while in the eel
and flounder extrarenal losses make up about 10% of the total (Tables 7.9 and 7.7).
In fish that are not feeding the accumulation of sodium is almost entirely accounted
for by the active uptake of sodium across the gills. KROGH (1939) depleted goldfish
222