124
A. M. PERKS
almost entirely to the freshwater lamprey, Lampetra fluviatilis, and they
have produced a number of negative results. The injection of pure arginine
vasotocin in doses of 36 mpmoles/kg failed to cause any water-balance
effect, and injections of 2.2 pg failed to change the volume of urine
production over a 6-hr period (Heller and Bentley, 1965; Bentley and
Follett, 1963). However, it is possible that the lamprey neurohypophysis
may influence sodium metabolism, and this is reminiscent of the possible
effects in the hagfish. The injection of a number of neurohypophysial
peptides, including arginine vasotocin, into the peritoneum of Lampetra
fluviutilis, resulted in an increase in the rate of sodium loss from the fish
into its external medium (Bentley and Follett, 1962, 1963). The site of
action was in part the kidney, since injection of arginine vasotocin increased the sodium and potassium concentrations of the urine, and it is
possible that a depression of tubular sodium reabsorption may be one
factor involved ( W. H. Sawyer, 1965a). Although all the peptides tested
provoked sodium loss, a comparison of equimolar doses suggested that
arginine vasotocin, the natural principle of the lamprey, was only one-fifth
as potent as mammalian oxytocin, on a weight basis. If comparisons were
made on the basis of the oxytocic activity which was injected, arginine
vasotocin was slightly less effective than oxytocin and considerably
weaker than the potent 4 Ser, 8 Ile oxytocin-which is the natural oxytocinlike peptide of the teleost fish. This unexpected weakness of arginine
vasotocin must lead to speculation on the possible existence of a neutral,
oxytocinlike peptide in the lamprey pituitary. This second peptide might
be present only during the marine period of existence, for Bentley and
Follett (1962) have suggested that the actions of the principles on sodium
metabolism would be of greatest use during the marine phase of the life
cycle. Further, Dodd et a2. (1966) have pointed out that the high doses
required to produce a sodium response could reflect a reduced tissue
sensitivity which had occurred when the lamprey first entered freshwater.
Morris (1960) has suggested that there is a breakdown of osmotic controls at this time. This could also be connected with the low levels of
neurohypophysial peptides found in pituitaries taken from lampreys
adapted to freshwater ( 1.2 mU/gland, Lampetra fluviatilis, Follett and
Heller, 1964a). In fact, the doses of neurohypophysial principles needed
to evoke a sodium loss are greater than the total hormonal activity available in the lamprey’s pituitary. However, it must be remembered that a
low hormone content in the pituitary does not necessarily imply a low rate
of loss into the circulation, since the stored peptide is only a reflection of
the balance between hypothalamic supply and pituitary loss. This same
consideration may account for the failure of experiments to demonstrate
a significant difference between glands dissected from lampreys living in
A. M. PERKS
almost entirely to the freshwater lamprey, Lampetra fluviatilis, and they
have produced a number of negative results. The injection of pure arginine
vasotocin in doses of 36 mpmoles/kg failed to cause any water-balance
effect, and injections of 2.2 pg failed to change the volume of urine
production over a 6-hr period (Heller and Bentley, 1965; Bentley and
Follett, 1963). However, it is possible that the lamprey neurohypophysis
may influence sodium metabolism, and this is reminiscent of the possible
effects in the hagfish. The injection of a number of neurohypophysial
peptides, including arginine vasotocin, into the peritoneum of Lampetra
fluviutilis, resulted in an increase in the rate of sodium loss from the fish
into its external medium (Bentley and Follett, 1962, 1963). The site of
action was in part the kidney, since injection of arginine vasotocin increased the sodium and potassium concentrations of the urine, and it is
possible that a depression of tubular sodium reabsorption may be one
factor involved ( W. H. Sawyer, 1965a). Although all the peptides tested
provoked sodium loss, a comparison of equimolar doses suggested that
arginine vasotocin, the natural principle of the lamprey, was only one-fifth
as potent as mammalian oxytocin, on a weight basis. If comparisons were
made on the basis of the oxytocic activity which was injected, arginine
vasotocin was slightly less effective than oxytocin and considerably
weaker than the potent 4 Ser, 8 Ile oxytocin-which is the natural oxytocinlike peptide of the teleost fish. This unexpected weakness of arginine
vasotocin must lead to speculation on the possible existence of a neutral,
oxytocinlike peptide in the lamprey pituitary. This second peptide might
be present only during the marine period of existence, for Bentley and
Follett (1962) have suggested that the actions of the principles on sodium
metabolism would be of greatest use during the marine phase of the life
cycle. Further, Dodd et a2. (1966) have pointed out that the high doses
required to produce a sodium response could reflect a reduced tissue
sensitivity which had occurred when the lamprey first entered freshwater.
Morris (1960) has suggested that there is a breakdown of osmotic controls at this time. This could also be connected with the low levels of
neurohypophysial peptides found in pituitaries taken from lampreys
adapted to freshwater ( 1.2 mU/gland, Lampetra fluviatilis, Follett and
Heller, 1964a). In fact, the doses of neurohypophysial principles needed
to evoke a sodium loss are greater than the total hormonal activity available in the lamprey’s pituitary. However, it must be remembered that a
low hormone content in the pituitary does not necessarily imply a low rate
of loss into the circulation, since the stored peptide is only a reflection of
the balance between hypothalamic supply and pituitary loss. This same
consideration may account for the failure of experiments to demonstrate
a significant difference between glands dissected from lampreys living in