may be envisaged as taking place by an alteration in th e configuration of structural
proteins and /or lipids in the cell membrane but there is no direct evidence about
this.
Alternatively such differences in osmotic and diffusion permeability could arise
as a result of the presence of 'long pores' (HARRIS , 1960). The molecules must 'line
up' , in file, so that the labelled ones present cross more slowly and so give a low
estimate of the rate of diffu sion. HAYS and FRANKl (1970) have shown that when
the fluid bathing each side of the toad bladder is stirred rapidly the estimated diffusion permeability in the presence of vasopressin actuall y increases as much as
10-fold.'They have suggested that the anomalous results obtained previously were
the result of a masking effect of unstirred layers of water and that these could be
synonymous with 'long pores'.
Sodium movement in response to neurohypophysial hormones is conceptually
even more difficult than that of water, as active transport is involved. This latter
process need not be directly related to the action of the hormones, as merely supplying the 'pump' with more of its ionic substrate could be sufficient to increase
its activit y. The effector mechanism for mediating the action of neurohypophysial
hormones on sodium transport across the bladder is physiologically distinct from
that concerned with water movement. This is apparent at all levels of the response.
At the primary receptor, various neurohypophysial peptides have relativel y different potencies in eliciting each response (BOURGUET and MAETZ, 1961). In the secondary reactions, the osmotic response is blocked by Ca 2+ and Mn 2+, but the increase in sodium transfer is unaffected (BENTLEY, 1960a and 1967; PETERSEN and
EDELMAN, 1964). The final effector mechanisms can exist independently, as shown
in the skins of the anuran, Xenopus laevis, and the urodele, Triturus alpestris, which
respond by increasing sodium, but not by water transfer,(MAETZ, 1963; BENTLEY
and HELLER, 1964). This distinction, between water and sodium effecrors, is important in assessing the nature of the change in permeability, and also with respect
to the evolution of the ph ysiological actions of these peptides.
Early experimental evidence suggested that the neurohypophysial hormones
increase the rate of admission of sodium into the cell, by increasing the permeability
of the membrane on the mucosal side. This evidence was based on the measurement
of changes in th e concentration of radioactively labelled sodium in the bladder
('sodium pool'). An increase in the level of labelled sodium was assumed to reflect
an increased rate of admission across the mucosal border into the cell. However,
there is now considerable uncertainty as to the distribution of the sodium throughout the bladder tissue, making such evidence equivocal (SHARP et al., 1966). CIVAN
and FRAZIER (1968) have impaled toad bladder epithelial cells on microelectrodes,
in order to measure the D. C. resistance across the mucosal cell border. They found
that after exposure to vasopressin, 98% of the decrease in D. C. resistance that is
observed across the whole membrane can be accounted for by the change at the
mucosal barrier. This is consistent with the earlier ideas about the site of the hormone's action .
P) Aldosterone. Aldosterone, as well as corticosterone and cortisol, increases
sodium transport across the toad bladder in vitro. Other steroid hormones, like
oestradiol and progesterone, lack this activity and may competitively inhibit the
85
proteins and /or lipids in the cell membrane but there is no direct evidence about
this.
Alternatively such differences in osmotic and diffusion permeability could arise
as a result of the presence of 'long pores' (HARRIS , 1960). The molecules must 'line
up' , in file, so that the labelled ones present cross more slowly and so give a low
estimate of the rate of diffu sion. HAYS and FRANKl (1970) have shown that when
the fluid bathing each side of the toad bladder is stirred rapidly the estimated diffusion permeability in the presence of vasopressin actuall y increases as much as
10-fold.'They have suggested that the anomalous results obtained previously were
the result of a masking effect of unstirred layers of water and that these could be
synonymous with 'long pores'.
Sodium movement in response to neurohypophysial hormones is conceptually
even more difficult than that of water, as active transport is involved. This latter
process need not be directly related to the action of the hormones, as merely supplying the 'pump' with more of its ionic substrate could be sufficient to increase
its activit y. The effector mechanism for mediating the action of neurohypophysial
hormones on sodium transport across the bladder is physiologically distinct from
that concerned with water movement. This is apparent at all levels of the response.
At the primary receptor, various neurohypophysial peptides have relativel y different potencies in eliciting each response (BOURGUET and MAETZ, 1961). In the secondary reactions, the osmotic response is blocked by Ca 2+ and Mn 2+, but the increase in sodium transfer is unaffected (BENTLEY, 1960a and 1967; PETERSEN and
EDELMAN, 1964). The final effector mechanisms can exist independently, as shown
in the skins of the anuran, Xenopus laevis, and the urodele, Triturus alpestris, which
respond by increasing sodium, but not by water transfer,(MAETZ, 1963; BENTLEY
and HELLER, 1964). This distinction, between water and sodium effecrors, is important in assessing the nature of the change in permeability, and also with respect
to the evolution of the ph ysiological actions of these peptides.
Early experimental evidence suggested that the neurohypophysial hormones
increase the rate of admission of sodium into the cell, by increasing the permeability
of the membrane on the mucosal side. This evidence was based on the measurement
of changes in th e concentration of radioactively labelled sodium in the bladder
('sodium pool'). An increase in the level of labelled sodium was assumed to reflect
an increased rate of admission across the mucosal border into the cell. However,
there is now considerable uncertainty as to the distribution of the sodium throughout the bladder tissue, making such evidence equivocal (SHARP et al., 1966). CIVAN
and FRAZIER (1968) have impaled toad bladder epithelial cells on microelectrodes,
in order to measure the D. C. resistance across the mucosal cell border. They found
that after exposure to vasopressin, 98% of the decrease in D. C. resistance that is
observed across the whole membrane can be accounted for by the change at the
mucosal barrier. This is consistent with the earlier ideas about the site of the hormone's action .
P) Aldosterone. Aldosterone, as well as corticosterone and cortisol, increases
sodium transport across the toad bladder in vitro. Other steroid hormones, like
oestradiol and progesterone, lack this activity and may competitively inhibit the
85