The intracellular sodium content, unidirectional radiosodium efflux, and unidirectional radiosodium influx were studied in whole rat tail arteries and in rat tail artery strips. The tissues were allowed to come to a steady condition while immersed in physiological salt solution at 37 degrees C, then were subjected to a small transient mechanical disturbance or to a larger disturbance of 5-20 min duration. The small transient disturbance caused a large transient increase in the sodium content of the cells, in the radiosodium influx, and in the radiosodium efflux. The sustained disturbance caused a sustained increase in sodium content. All effects of a mechanical disturbance were prevented by blockade of alpha-adrenoreceptors with 1 microM phenoxybenzamine. Pre-treatment of the rat with reserpine was as effective as acute treatment of the artery with phenoxybenzamine in preventing the transient increase in the radiosodium efflux. It is hypothesized that mechanical disturbances cause norepinephrine release from terminal adrenergic plexuses in the artery wall, and that the binding of norepinephrine to alpha-adrenoreceptors in the smooth muscle cells causes an increase in the sodium permeability of the cell membrane.