Slow wave potentials (SWPs) are transient depolarizations which propag
ate substantial distances from their point of origin. They were induce
d in the epidermal cells of pea epicotyls by injurious methods such as
root excision and heat treatment, as well as by externally applied, d
efined steps in xylem pressure (P-x) in the absence of wounding. The c
ommon principle of induction was a rapid increase in P-x. Such a stimu
lus appeared under natural conditions after (i) bending of the epicoty
l, (ii) wounding of the epidermis, (iii) rewatering of dehydrated root
s, and (iv) embolism. The induced depolarization was not associated wi
th a change in cell input resistance. This result and the ineffectiven
ess of ion channel blockers point to H+-pumps rather than ion channels
as the ionic basis of the SWP. Stimuli such as excision, heat treatme
nt and pressure steps, which generate SWPs, caused a transient increas
e in the fluorescence intensity of epicotyls loaded with the pH-indica
tor DM-NERF, a 2', 7'-dimethyl derivative of rhodol, but not of those
loaded with the pH indicator -bis-(2-carboxyethyl)-5-(and-6)-carboxyfl
uorescein (BCECF). Matching kinetics of depolarization and pH response
identify a transient inactivation of proton pumps in the plasma membr
ane as the causal mechanism of the SWP. Feeding pump inhibitors to the
cut surface of excised epicotyls failed to chemically simulate a SWP;
cyanide, azide and 2,4-dinitrophenol caused sustained, local depolari
zations which did not propagate. Of all tested substances, only sodium
cholate caused a transient and propagating depolarization whose arriv
al in the growing region of the epicotyl coincided with a transient gr
owth rate reduction.