fluid with the aid of micropipettes such as are used in experiments with mammals
and amphibians.
a ) The Urinary Bladder. Man y fish have a urinary bladder that originates as an
expansion of the mesonephric ducts. When the composition of the urine stored in
such receptacles is compared with that collected directly from the ureters, differences in composition are apparent. In the flounder the sodium chloride levels are
lower in the bladder urine of fish in either fresh water or sea-water (Lo\HLOU, 1967).
This seems to result from reabsorption of these ions, which in sea-water leads to
additional water conservation and in fresh water to a further saving of sodium chloride. LAHLOU et. al. (1969 b) have also found evidence for such ionic reabsorption
from the urinary bladder of the toadfish.
fl) Neurohypophysial Peptides and Adrenocorticosteroids.The injection of various
neurohypophysial peptides can influence renal sodium excretion in some fish.Vasotocin has been shown to increase renal sodium losses in goldfish, eels, the African
lungfish and lampreys (Table 7.8). Isotocin also has this action in eels, but in goldfish
it sometimes produces a renal sodium retention. Such peptides do not, however,
invariably alter renal sodium losses in fish while the physiological significance of
such an action, when it does occur, is unknown. The increases in renal sodium excretion result (except in the lamprey) from increas es in the GFR. The adrenocorticosteroids appear, in contrast to their effects on the gills, to be without an action
on the sodium and potassium content of the urine (Table 7.10). This is in contrast
to the actions of such steroids in the higher tetrapods, but is reminiscent of the failure to demonstrate such an action in amphibians.
c) The Gut
The intestine of fish living in fresh water actively transports sodium from the lumen
to the blood. SMITH (1964; 1966) found that sodium and potassium moved from
the fluid bathing the mucosal surface of isolated sacs of the goldfish intestine.
Sodium transport greatly exceeded that of potassium and resulted in the generation
of an electrical p. d., serosal side positive, of about 7 mV across the membrane. The
process is inhibited by a Na-K ATPase inhibitor, ouabain, and the enzyme has been
isolated and histologically identified in the mucosal epithelial cells lining the intestine (M. SMITH, 1967; HOLLANDS and SMITH, 1964). The level of the Na-K activated ATPase in the goldfish intestine is labile, as also seen in marine teleosts.
When the fish were kept in water at 8
0 the activity of the enzyme increased to
about twice the level seen when they were maintained at 30
0
• This may reflect the
operation of a mechanism for controlling the rate of sodium absorption at different
temperatures, similar to that influencing the levels of this enzyme in fish kept in
sea-water.
The relative importance of sodium chloride absorption from the gut and gills
of freshwater fish probably varies in different conditions. Fasting fish in fresh water
are expected to gain little sodium from the water that the y drink, as this usually contains less than 1 m-equiv/l . Less than 0.5% of the total sodium accumulated by the
226
and amphibians.
a ) The Urinary Bladder. Man y fish have a urinary bladder that originates as an
expansion of the mesonephric ducts. When the composition of the urine stored in
such receptacles is compared with that collected directly from the ureters, differences in composition are apparent. In the flounder the sodium chloride levels are
lower in the bladder urine of fish in either fresh water or sea-water (Lo\HLOU, 1967).
This seems to result from reabsorption of these ions, which in sea-water leads to
additional water conservation and in fresh water to a further saving of sodium chloride. LAHLOU et. al. (1969 b) have also found evidence for such ionic reabsorption
from the urinary bladder of the toadfish.
fl) Neurohypophysial Peptides and Adrenocorticosteroids.The injection of various
neurohypophysial peptides can influence renal sodium excretion in some fish.Vasotocin has been shown to increase renal sodium losses in goldfish, eels, the African
lungfish and lampreys (Table 7.8). Isotocin also has this action in eels, but in goldfish
it sometimes produces a renal sodium retention. Such peptides do not, however,
invariably alter renal sodium losses in fish while the physiological significance of
such an action, when it does occur, is unknown. The increases in renal sodium excretion result (except in the lamprey) from increas es in the GFR. The adrenocorticosteroids appear, in contrast to their effects on the gills, to be without an action
on the sodium and potassium content of the urine (Table 7.10). This is in contrast
to the actions of such steroids in the higher tetrapods, but is reminiscent of the failure to demonstrate such an action in amphibians.
c) The Gut
The intestine of fish living in fresh water actively transports sodium from the lumen
to the blood. SMITH (1964; 1966) found that sodium and potassium moved from
the fluid bathing the mucosal surface of isolated sacs of the goldfish intestine.
Sodium transport greatly exceeded that of potassium and resulted in the generation
of an electrical p. d., serosal side positive, of about 7 mV across the membrane. The
process is inhibited by a Na-K ATPase inhibitor, ouabain, and the enzyme has been
isolated and histologically identified in the mucosal epithelial cells lining the intestine (M. SMITH, 1967; HOLLANDS and SMITH, 1964). The level of the Na-K activated ATPase in the goldfish intestine is labile, as also seen in marine teleosts.
When the fish were kept in water at 8
0 the activity of the enzyme increased to
about twice the level seen when they were maintained at 30
0
• This may reflect the
operation of a mechanism for controlling the rate of sodium absorption at different
temperatures, similar to that influencing the levels of this enzyme in fish kept in
sea-water.
The relative importance of sodium chloride absorption from the gut and gills
of freshwater fish probably varies in different conditions. Fasting fish in fresh water
are expected to gain little sodium from the water that the y drink, as this usually contains less than 1 m-equiv/l . Less than 0.5% of the total sodium accumulated by the
226