Numerous measurements of sodium fluxes in the presence of aldosterone indicate that the increased net flux results from facilitated influx from mucosa to serosa, and not a decrease of movement in the opposite direction. The possibility
that aldosterone increases the rate of admission of sodium across the mucosal surface into the cell has received serious consideration based originally on measurements of the isotopic sodium 'pool' in the tissue. As mentioned previously, uncertainties about the precise location of this sodium make such results difficult to
interpret. However, indirect evidence involving possible analogies between the
action of aldosterone and that of amphotericin B (which destroys the selectivity
of the mucosal border and admits sodium into the cell) suggests that this mode
of action is possible (SHARP and LEAF, 1968). The protein induced by aldosterone
could be a permease. EDELMAN and his collaborators do not consider this explanation likely (FIMOGNARI, PORTER, and EDELMAN, 1967; FANESTIL, PORTER,
and EDELMAN, 1967) as they found that aldosterone increases the electromotive
force of the sodium 'pump' and this is related to the levels of certain substrates
in the tricarboxylic acid cycle. Furthermore CUTHBERT and PAINTER (1969) have
found that when they abolish sodium transport across the toad bladder by exposing
it to ouabain, but maintain the p.d. by passing a current through the membrane,
the electrical properties of the membrane are unaltered by aldosterone. Vasopressin
on the other hand was still effective under these conditions. CUTHBERT and PAINTER
consider that if a permease, which acts on the mucosal membrane of the epithelial
cells, were involved, its action, like that of vasopressin, should still be apparent.
The proteins induced by aldosterone may then be enzymes that effect energy substrate levels, and eventually facilitate the formation of ATP. The activity of certain
enzymes, involved in the tricarboxylic acid cycle, increase in the presence of aldosterone, and this effect is independent of the presence of sodium (KIRSTEN et al., 1968).
KIRSTEN et al. do not consider that their results rule out a parallel action of the
hormone on sodium entry into the cell, but suggest that the two effects could occur
together and be mutually supportive.
87
that aldosterone increases the rate of admission of sodium across the mucosal surface into the cell has received serious consideration based originally on measurements of the isotopic sodium 'pool' in the tissue. As mentioned previously, uncertainties about the precise location of this sodium make such results difficult to
interpret. However, indirect evidence involving possible analogies between the
action of aldosterone and that of amphotericin B (which destroys the selectivity
of the mucosal border and admits sodium into the cell) suggests that this mode
of action is possible (SHARP and LEAF, 1968). The protein induced by aldosterone
could be a permease. EDELMAN and his collaborators do not consider this explanation likely (FIMOGNARI, PORTER, and EDELMAN, 1967; FANESTIL, PORTER,
and EDELMAN, 1967) as they found that aldosterone increases the electromotive
force of the sodium 'pump' and this is related to the levels of certain substrates
in the tricarboxylic acid cycle. Furthermore CUTHBERT and PAINTER (1969) have
found that when they abolish sodium transport across the toad bladder by exposing
it to ouabain, but maintain the p.d. by passing a current through the membrane,
the electrical properties of the membrane are unaltered by aldosterone. Vasopressin
on the other hand was still effective under these conditions. CUTHBERT and PAINTER
consider that if a permease, which acts on the mucosal membrane of the epithelial
cells, were involved, its action, like that of vasopressin, should still be apparent.
The proteins induced by aldosterone may then be enzymes that effect energy substrate levels, and eventually facilitate the formation of ATP. The activity of certain
enzymes, involved in the tricarboxylic acid cycle, increase in the presence of aldosterone, and this effect is independent of the presence of sodium (KIRSTEN et al., 1968).
KIRSTEN et al. do not consider that their results rule out a parallel action of the
hormone on sodium entry into the cell, but suggest that the two effects could occur
together and be mutually supportive.
87