2. THE NEUROHYPOPHYSIS
175
1963; Anguilla anguilla, Sharratt et al., 1964). However, the diuresis, and
its concomitant sodium loss are transitory, and they are outlasted by more
profound affects on sodium movement in and out of the fish at extrarenal
sites such as the gills (Carmsius auratus; Maetz and Julien, 1961; Maetz,
1963). In freshwater fish, such as Carassius auratus, it has been shown
that oxytocin and 4 Ser, 8 Ile oxytocin stimulate influx of sodium, probably at the gills, while arginine vasotocin will enhance both influx and
outfiux (Maetz, 1963; Maetz et al., 1964). In the marine fish, such as
Platichthys fleszcs, oxytocin increased sodium outflux, and arginine vasotocin was potent in promoting rapid sodium exchanges (Maetz, 1963;
Motais and Maetz, 1964, 1987). Lysine vasopressin had little or no potency in these tests. These results can be summarized by saying that
neurohypophysial principles ( except lysine vasopressin) enhanced sodium
fluxes against the prevailing osmotic gradients; they accelerated the
process of adaptation to an environment of higher salinity (Maetz, 1963;
Motais and Maetz, 1967).
It is possible that diuretic responses in teleost fish result from general
vascular effects of the neurohypophysial peptides. There has been little
work on possible circulatory effects of these principles in teleosts. However, recently Lahlou et al. (1968) have found pressor effects in Opsanus
tau, after the injection of low, possibly physiological doses of arginine
vasotocin (5 nglkg ) , They obtained a good log dose-response curve from
their injections.
Maetz (1963) has pointed out the importance of avoiding shock or
“stress” effects, which often cause a “laboratory” diuresis during experiments on salt-water balance in teleosts. “Stresses” such as hypoxaemia or
handling are known to result in histological changes, with depletion or
accumulation of neurosecretion in the neurohypophysis ( Salmo gairdneri,
Carlson and Holmes, 1962; Ameiurus nebulosus, Molnar and Szabo, 1967;
Anguilla anguilla, Leatherland, 1967, Leatherland and Dodd, 1969b ) .
Since Stevens and Randall (1968; Stevens, 1968) have shown that in
Salmo gairdneri, adrenal medullary hormones may be liberated as a physiological mechanism for the control of the circulation during moderate
or strong exercise, it would be interesting to know whether neurohypophysial principles are liberated in the same circumstances. Perhaps
such moderate levels of “stress” could cause the release of neurohypophysial peptides; these might help in controlling sodium fluxes across the gills
during the rapid water movement which must occur during respiratory
activation owing to exercise.
Adrenal cortical tissue could also be involved in conditions of “stress”
and in sodium balance. It is interesting to find that Rasquin and Stoll
( 1957 ) have shown that injections of mammalian arginine-lysine vaso-
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