Stem elongatfon in peas (Pisum sativum L.) is under partial control by gibberellins, yet the mechanism of such control is uncertain. In this study, we examined the cellular and physical properties that govem stem elongation, to determine how gibberellins influence pea stem growth. Stem elongation of etiolated seedlings was retarded with uniconozol, a gibberellin synthesis inhibitor, and the growth retardation was reversed by exogenous gibberellin. Using the pressure probe and vapor pressure osmometry, we found little effect of uniconozol and gibberellin on cell turgor pressure or osmotic pressure. In contrast, these treatments had major effects on in vivo stress relaxation, measured by turgor relaxation and pressure-block techniques. Uniconozoltreated plants exhibited reduced wall relaxation (both initial rate and total amount). The results show that growth retardation is effected via a reduction in the wall yield coefficient and an increase in the yield threshold. These effects were largely reversed by exogenous gibberellin. When we measured the mechanical characteristics of the wall by stress/strain (Instron) analysis, we found only minor effects of uniconozol and gibberellin on the plastic compliance. This observation indicates that these agents did not alter wall expansion through effects on the mechanical (viscoelastic) properties of the wall. Our results suggest that wall expansion in peas is better viewed as a chemorheological, rather than a viscoelasfic, process.Gibberellins were discovered because of their marked stimulation of shoot elongation. In recent years notable progress has been made in the genetics of gibberellin synthesis and its control of shoot elongation, particularly in pea and maize plants (see Ref. 20 for review). However, the mechanism of action of GA on shoot growth in these species is not fully understood. Two general, and complementary, approaches have been taken to examine GA action. The first views the stem as composed of cell files, and asks how GA affects the number and final size ofthe cells making up the stem. Various studies (e.g. 24, 26) have shown that GA may affect both cell division and final cell size. However, final cell size is a complex function of the patterns of cell expansion and cell division, which are themselves likely to be interdependent, so the causal mechanism of GA action is not clear from these studies. The second approach considers that stem elongation '