differences in ionic concentration were measured. Also, the
chemical potential gradients between the apoplast and the
cytosol of stem tissue cells would not be conducive to rapid
passive effluxes of Ca2+ and Mg2+ and an influx of K+, as
was suggested by the time course trends in concentration.
The pool of Ca2+ and Mg2’ contributing to the concentration
increase within the xylem solution upon foliar treatment
with t(+)-adenosine could not be determined from this study.
One potential pool of cations might be the extracellular
Donnan phase within the cell wall and the externa1 surface
of the plasma membrane (Demarty et al., 1984). The cell wall
in stem tissue has a relatively high cation exchange capacity
due to the large amount of xylem tissue. A release of Ca2+
and Mg2+ into the solution phase might be the result of
acidification of the apoplast. Alternatively, an intracellular
pool of Ca2+, which could supply Caz+ indirectly to the
apoplast, might be the ER (Buckhout, 1984). Transport of the
Ca2+ from the ER to the apoplast would necessitate movement
across two membranes and, thus, would be expected
to be relatively slow.
The mechanism by which L(+)-adenosine elicits a recompartmentation
of cations within stem tissue is not evident. It
is also quite puzzling as to why an exogenous application of
D(-)-adenosine has an inhibitory effect on this response
when D(-)-adenosine is the predominant endogenous form
of adenosine in plants. In rice roots, for example, approximately
99% of the 125 pg of adenosine g-’ dry weight present
within the tissue is in the form of D(-)-adenosine (Ries, 1991).
A similar situation exists with TRIA, which is inhibited by
octacosanol at concentrations of 10-l’ M or less when they
are applied together exogenously (Jones et al., 1979). Octacosanol
is the predominant long chain alcohol in plants. The
most obvious explanation for the lack of an apparent inhibitory
effect of endogenous D(-)-adenosine would be that it is
localized within a subcellular compartment that is distinct
from the site of action of the exogenously applied L(+)-
adenosine.