those from areas where they have fresh water to drink (HOLMES, BUTLER, and PHILLIPS, 1961). These differences are thought to reflect the sodium content of the diet.
Young gulls given sodium chloride solutions to drink develop larger adrenal glands
than gulls provided with fresh water. HOLMES and his collaborators have suggested
that this may reflect a greater need for corticosteroids, in order to facilitate the excretion of salt from the nasal glands of such bird s. The young gulls provided with
saline solutions to drink grew less rapidly than the birds with fresh water. The same
has also been obs erved in ducklings on such a regimen (SCHMIDT-NIELSEN and
KIM, 1964). Administration of corticosteroids to young rats inhibits their growth
(see HARTMAN and BROWNELL, 1949), so that the observations on birds suggest
an enhanced rate of secretion of corticosteroids. The circulating steroid levels in
such young birds, however, have not been determined. As we have seen, ad ult ducks
provided with saline solutions to drink have corticosterone levels in their plasma
similar to those of birds given fresh water (DONALDSON and HOLMES, 1965). The
adrenal tissues from these two groups of ducks also produce similar amounts of
corticosterone and aldosterone in vitro , but as the birds given saline have additional
tissue, they potentially can produce more of the hormones.
The physiological significance of the relationships of the weight of the adrenal
gland s to the salt content of the diet, and the role of corticosteroids in the electrolyte
metabolism in birds are not clear. In mammals, corticosteroids mediate sodium
retention and conservation, but in birds the y have two postulated roles in sodium
metabolism that are opposite in effect, retention by the kidneys and excretion by
the nasal glands. Numerous species of birds lack functional nasal glands and so
presumably only utilize corticosteroids to mediate renal sodium conservation.
Others, such as marine species, could use the hormones mainly to facilitate sodium
excretion through the nasal glands. Yet others (like ducks) conceivably could require either process, depending on the dietary circumstances.
The role of the adrenocortical hormones in sodium metabolism of birds thus
appears to be in a somewhat schizophrenic state as they ma y produce retention
or excretion of sodium. One rationalization of this paradox would be that these hormones have a different role in marine sodium-replete species with nasal salt glands,
from that in terrestrial spec ies which potentially suffer sodium depletion. Intuitively I find this difficult to believe, principally because it also requires a complete realignment in the stimuli that inititiate discharge of th e steroids. The usual
stimulus for corticosteroid release in vertebrates is a decreased sodium level resulting in a reduction of plasma volume. A large sodium intake will have an inh ibitory
effect on this. However, we must conclude either that th e available information
has been misinterpreted or a novel and un ique mechanism controlling release of
corticosteroids exists in at least some birds that ut ilize it to promote sodium excretion. I would hesitantly make two suggestions. First, that adrenal hypertrophy
seen in young sodium-replete birds is the result of excessive secretion of corticotrophin resulting from a depression of the inhibitory action of circulating corticosteroids on the adenohypophysis. Second, that normal basal levels of corticosteroids
in the plasma are adequate to maintain the integrity of the secretory mechanisms
in the nasal gland, provided there is assistance by a vasodilatation in this tissue.
127
Young gulls given sodium chloride solutions to drink develop larger adrenal glands
than gulls provided with fresh water. HOLMES and his collaborators have suggested
that this may reflect a greater need for corticosteroids, in order to facilitate the excretion of salt from the nasal glands of such bird s. The young gulls provided with
saline solutions to drink grew less rapidly than the birds with fresh water. The same
has also been obs erved in ducklings on such a regimen (SCHMIDT-NIELSEN and
KIM, 1964). Administration of corticosteroids to young rats inhibits their growth
(see HARTMAN and BROWNELL, 1949), so that the observations on birds suggest
an enhanced rate of secretion of corticosteroids. The circulating steroid levels in
such young birds, however, have not been determined. As we have seen, ad ult ducks
provided with saline solutions to drink have corticosterone levels in their plasma
similar to those of birds given fresh water (DONALDSON and HOLMES, 1965). The
adrenal tissues from these two groups of ducks also produce similar amounts of
corticosterone and aldosterone in vitro , but as the birds given saline have additional
tissue, they potentially can produce more of the hormones.
The physiological significance of the relationships of the weight of the adrenal
gland s to the salt content of the diet, and the role of corticosteroids in the electrolyte
metabolism in birds are not clear. In mammals, corticosteroids mediate sodium
retention and conservation, but in birds the y have two postulated roles in sodium
metabolism that are opposite in effect, retention by the kidneys and excretion by
the nasal glands. Numerous species of birds lack functional nasal glands and so
presumably only utilize corticosteroids to mediate renal sodium conservation.
Others, such as marine species, could use the hormones mainly to facilitate sodium
excretion through the nasal glands. Yet others (like ducks) conceivably could require either process, depending on the dietary circumstances.
The role of the adrenocortical hormones in sodium metabolism of birds thus
appears to be in a somewhat schizophrenic state as they ma y produce retention
or excretion of sodium. One rationalization of this paradox would be that these hormones have a different role in marine sodium-replete species with nasal salt glands,
from that in terrestrial spec ies which potentially suffer sodium depletion. Intuitively I find this difficult to believe, principally because it also requires a complete realignment in the stimuli that inititiate discharge of th e steroids. The usual
stimulus for corticosteroid release in vertebrates is a decreased sodium level resulting in a reduction of plasma volume. A large sodium intake will have an inh ibitory
effect on this. However, we must conclude either that th e available information
has been misinterpreted or a novel and un ique mechanism controlling release of
corticosteroids exists in at least some birds that ut ilize it to promote sodium excretion. I would hesitantly make two suggestions. First, that adrenal hypertrophy
seen in young sodium-replete birds is the result of excessive secretion of corticotrophin resulting from a depression of the inhibitory action of circulating corticosteroids on the adenohypophysis. Second, that normal basal levels of corticosteroids
in the plasma are adequate to maintain the integrity of the secretory mechanisms
in the nasal gland, provided there is assistance by a vasodilatation in this tissue.
127