similar to those following administration of hyperosmotic solutions. The effects
of either nerve stimulation or hyperosmotic solutions, could be blocked by injecting atropine which is a peripheral parasympathetic blocking agent. Secretion
could also be induced with parasympathomimetic drugs such as acetylcholine. ASH,
PEARCE, and SILVER (1969) have recently extended these observations in ducks.
Stimulation of nasal gland secretion by infusion of hyperosmotic saline solutions
was abolished when th e nerve supply to the gland was excised . This clearly indicates
that adrenocorticosteroids are not directly involved in the initiation of secretion.
Furthermore the injection of carbachol can initiate secretion in such ducks. If the
nerve is cut on the central side of its ganglion, or if transmission through this tissue
is blocked by hexamethonium the response could still be initiated. This suggests
that the receptors are not located in the central nervous system but possibly within
the ganglion itself . All of these observations clearl y indicate that the response is
directly initiated by the parasympathetic nerves, probably through a reflex initiated
at an osmoreceptor site somewhere in the nerve tract proximal to the gland.
The overall control of nasal gland secretion is probably more complex than this,
and appears to involve also the adrenocorticosteroid hormones. PHILLIPS et at.
(1961) found that when ducks were adrenalectomized, initiation of nasal salt gland
secretion in response to administration of saline solutions was abolished. However,
if the birds were maintained with daily injections of cortisol they responded in the
usual way. Adrenalectomy is a traumatic procedure that adversely affects a multitude of body functions, but it was also found that injections of cortisol, aldosterone and corticotrophin into normal ducks potentiated salt gland secretion
(HOLMES, PHILLIPS, and BUTLER, 1961). Cortisol is not normally present in ducks
and the actions of aldosterone are probably an indirect result of elevated plasma
sodium levels due to a prominent renal action (PHILLIPS and BELLAMY, 1962). Corticosterone, which occurs naturally in high concentrations in duck plasma, also
stimulates nasal salt gland secretion in saline-loaded ducks (HOLMES, PHILLIPS, and
CHESTER JONES, 1963), but the levels of this steroid in the blood do not change
when the birds are given such saline loads (DONALDSON and HOLMES, 1956; MACCHI et al., 1965). This latter observation is difficult to reconcile with a primary excitatory action of these steroids on nasal gland secretion. When saline solution is
given to ducks the extracellular (inulin) space of the nasal glands doubles, and it
has been suggested that th is may afford the tissue an added opportunity to react
with the circulating corticosteroids (BELLAMY and PHILLIPS, 1966).
The blood flow through the nasal glands of ducks and gulls increases during
secretion; this probably accounts for the increased inulin space referred to above
(FANGE, KROG , and REITE, 1963). This effect is mediated partly by the parasympathetic stimulation, and possibly also by local vasodilators like carbon dioxide
and kinin-like substances. FANGE et at. have shown that this vasodilatation is secondary to the onset of secretion. However, it ma y play an important part in the
process, as SCHMIDT-NIELSE N'S group found that adrenaline, which has a vasoconstrictor action, reduced the response of the nasal gland . It is also interesting
that when the rates of nasal gland secretion are reduced in herring gulls following
deprivation of water, secretion can be increased by the injection of adrenergic
blocking agents that promote vasodilatation (DOUGLAS and NEE!.:Y, 1969). It is possible that increased access of corticosteroids, during such vasodilatation, ma y play
124
of either nerve stimulation or hyperosmotic solutions, could be blocked by injecting atropine which is a peripheral parasympathetic blocking agent. Secretion
could also be induced with parasympathomimetic drugs such as acetylcholine. ASH,
PEARCE, and SILVER (1969) have recently extended these observations in ducks.
Stimulation of nasal gland secretion by infusion of hyperosmotic saline solutions
was abolished when th e nerve supply to the gland was excised . This clearly indicates
that adrenocorticosteroids are not directly involved in the initiation of secretion.
Furthermore the injection of carbachol can initiate secretion in such ducks. If the
nerve is cut on the central side of its ganglion, or if transmission through this tissue
is blocked by hexamethonium the response could still be initiated. This suggests
that the receptors are not located in the central nervous system but possibly within
the ganglion itself . All of these observations clearl y indicate that the response is
directly initiated by the parasympathetic nerves, probably through a reflex initiated
at an osmoreceptor site somewhere in the nerve tract proximal to the gland.
The overall control of nasal gland secretion is probably more complex than this,
and appears to involve also the adrenocorticosteroid hormones. PHILLIPS et at.
(1961) found that when ducks were adrenalectomized, initiation of nasal salt gland
secretion in response to administration of saline solutions was abolished. However,
if the birds were maintained with daily injections of cortisol they responded in the
usual way. Adrenalectomy is a traumatic procedure that adversely affects a multitude of body functions, but it was also found that injections of cortisol, aldosterone and corticotrophin into normal ducks potentiated salt gland secretion
(HOLMES, PHILLIPS, and BUTLER, 1961). Cortisol is not normally present in ducks
and the actions of aldosterone are probably an indirect result of elevated plasma
sodium levels due to a prominent renal action (PHILLIPS and BELLAMY, 1962). Corticosterone, which occurs naturally in high concentrations in duck plasma, also
stimulates nasal salt gland secretion in saline-loaded ducks (HOLMES, PHILLIPS, and
CHESTER JONES, 1963), but the levels of this steroid in the blood do not change
when the birds are given such saline loads (DONALDSON and HOLMES, 1956; MACCHI et al., 1965). This latter observation is difficult to reconcile with a primary excitatory action of these steroids on nasal gland secretion. When saline solution is
given to ducks the extracellular (inulin) space of the nasal glands doubles, and it
has been suggested that th is may afford the tissue an added opportunity to react
with the circulating corticosteroids (BELLAMY and PHILLIPS, 1966).
The blood flow through the nasal glands of ducks and gulls increases during
secretion; this probably accounts for the increased inulin space referred to above
(FANGE, KROG , and REITE, 1963). This effect is mediated partly by the parasympathetic stimulation, and possibly also by local vasodilators like carbon dioxide
and kinin-like substances. FANGE et at. have shown that this vasodilatation is secondary to the onset of secretion. However, it ma y play an important part in the
process, as SCHMIDT-NIELSE N'S group found that adrenaline, which has a vasoconstrictor action, reduced the response of the nasal gland . It is also interesting
that when the rates of nasal gland secretion are reduced in herring gulls following
deprivation of water, secretion can be increased by the injection of adrenergic
blocking agents that promote vasodilatation (DOUGLAS and NEE!.:Y, 1969). It is possible that increased access of corticosteroids, during such vasodilatation, ma y play
124