Characean internodal cells generate receptor potential (DeltaE (m)) in response to mechanical stimuli. Upon a long-lasting stimulus, the cells generated DeltaE (m) at the moment of both compression and decompression, and the amplitude of DeltaE (m) at the moment of decompression, (DeltaE (m))(E), was larger than that at compression. The long-lasting stimulus caused a membrane deformation (DeltaD (m)) having two components, a rapid one, (DeltaD (m))(rapid), at the moment of compression and a slower one, (DeltaD (m))(slow), during the long-lasting compression. We assumed that (DeltaD (m))(slow) might have some causal relation with the larger DeltaE (m) at (DeltaE (m))(E). We treated internodal cells with either HgCl(2) or ZnCl(2), water channel inhibitors, to decrease (DeltaD (m))(slow). Both inhibitors attenuated (DeltaD (m))(slow) during compression. Cells treated with HgCl(2) generated smaller (DeltaE (m))(E) compared to nontreated cells. On the other hand, cells treated with ZnCl(2) never attenuated (DeltaE (m))(E) but, rather, amplified it. Thus, the amplitude of (DeltaD (m))(slow) did not always show tight correlation with the amplitude of (DeltaE (m))(E). Furthermore, when a constant deformation was applied to an internodal cell in a medium with higher or lower osmotic value, a cell having higher turgor always showed a larger (DeltaE (m))(E). Thus, we concluded that changes in tension at the membrane may be the most important factor to induce activation of mechanosensitive Ca(2+) channel.