214
J. N. BALL
which the fall in plasma electrolytes after hypophysectomy is very marked
(from about 135-87 mEq/ liter plasma sodium; for example, Lahlou and
Sawyer, 1967), it would seem that the paralactin-based mechanism is
important for normal electrolyte control, but that the fish tissues are able
to tolerate large changes in the electrolyte composition of the body fluids.
The examples of the eel and the goldfish serve to warn us against
being overly impressed by the notion of failure in freshwater after hypophysectomy as being a necessary index or sign that a prolactin-based
mechanism normally operates. It so happens, because of ease of observation, that the facts of failure in freshwater after hypophysectomy, and its
correction by prolactin, were the salient points observed in the earlier
work; and some authors (including Ball, 1965a) have been misled by this
into postulating a unitary pituitary mechanism that operates to guarantee
survival in freshwater (or hypotonic media) with the implication that
this mechanism must be absent in species in which freshwater survival
is not impaired by hypophysectomy (see Schreibman and Kallman, 1966).
It has even been suggested that paralactin can play no role in a fish in
seawater, and that the 7 cells (see chapter by Ball and Baker, Volume 11)
must turn to the secretion of some other factor in seawater (Sage, 1968).
It is now apparent that we are actually dealing with something more
subtle than a kind of all-or-nothing survival mechanism, and we need to
think not in terms of life and death but of modulation of electrolyte
(especially sodium) movements across the body surface. As will be seen,
hypophysectomy and prolactin influence these sodium movements in the
same manner whether P. Zutipinna is in freshwater (where the pituitary is
essential for survival) or in dilute seawater (where the gland is not essential for survival).
It is probable that the major site of action of prolactin in relation to
sodium conservation in freshwater is on the passive outflux of sodium
from the body, presumably mainly at the gill. In F . heteroclitus and P.
latipinna, hypophysectomy results in a marked increase in sodium outflux
in freshwater which is corrected by prolactin (Maetz et al., 196%; Ensor
and Ball, 1968b), but not by cortisol in the latter species (Ensor and
Ball, 1968b). These changes are largely extrarenal in the killifish (Maetz
et al., 198%; Potts and Evans, 1966), and we assume that this is true also
in Poecilia. In the eel, too, we have seen that it is the sodium outflux that
is affected by hypophysectomy and prolactin, and the same probably applies to the goldfish. In P. Zutipinna living in a dilute seawater with
approximately the same sodium content as the plasma, the sodium turnover rate (i.e., percentage of exchangeable sodium leaving the body in
unit time) is strongly enhanced by hypophysectomy and is restored to
normal by chronic prolactin treatment, although not by an otherwise
J. N. BALL
which the fall in plasma electrolytes after hypophysectomy is very marked
(from about 135-87 mEq/ liter plasma sodium; for example, Lahlou and
Sawyer, 1967), it would seem that the paralactin-based mechanism is
important for normal electrolyte control, but that the fish tissues are able
to tolerate large changes in the electrolyte composition of the body fluids.
The examples of the eel and the goldfish serve to warn us against
being overly impressed by the notion of failure in freshwater after hypophysectomy as being a necessary index or sign that a prolactin-based
mechanism normally operates. It so happens, because of ease of observation, that the facts of failure in freshwater after hypophysectomy, and its
correction by prolactin, were the salient points observed in the earlier
work; and some authors (including Ball, 1965a) have been misled by this
into postulating a unitary pituitary mechanism that operates to guarantee
survival in freshwater (or hypotonic media) with the implication that
this mechanism must be absent in species in which freshwater survival
is not impaired by hypophysectomy (see Schreibman and Kallman, 1966).
It has even been suggested that paralactin can play no role in a fish in
seawater, and that the 7 cells (see chapter by Ball and Baker, Volume 11)
must turn to the secretion of some other factor in seawater (Sage, 1968).
It is now apparent that we are actually dealing with something more
subtle than a kind of all-or-nothing survival mechanism, and we need to
think not in terms of life and death but of modulation of electrolyte
(especially sodium) movements across the body surface. As will be seen,
hypophysectomy and prolactin influence these sodium movements in the
same manner whether P. Zutipinna is in freshwater (where the pituitary is
essential for survival) or in dilute seawater (where the gland is not essential for survival).
It is probable that the major site of action of prolactin in relation to
sodium conservation in freshwater is on the passive outflux of sodium
from the body, presumably mainly at the gill. In F . heteroclitus and P.
latipinna, hypophysectomy results in a marked increase in sodium outflux
in freshwater which is corrected by prolactin (Maetz et al., 196%; Ensor
and Ball, 1968b), but not by cortisol in the latter species (Ensor and
Ball, 1968b). These changes are largely extrarenal in the killifish (Maetz
et al., 198%; Potts and Evans, 1966), and we assume that this is true also
in Poecilia. In the eel, too, we have seen that it is the sodium outflux that
is affected by hypophysectomy and prolactin, and the same probably applies to the goldfish. In P. Zutipinna living in a dilute seawater with
approximately the same sodium content as the plasma, the sodium turnover rate (i.e., percentage of exchangeable sodium leaving the body in
unit time) is strongly enhanced by hypophysectomy and is restored to
normal by chronic prolactin treatment, although not by an otherwise