Rhythmic mechanical activity was recorded in vitro in isolated rat tail arteries. Pressurized cylindrical segments of this artery, stretched to their in situ length, exhibit well-synchronized rhythmic contractions. Frequency and amplitude of the rhythmic activity can be modified by (1) passive stretch at a given constrictor agonist concentration, as well as by (2) active wall stress changes induced by varying doses of constrictor agonists. At a norepinephrine concentration of 0.5 µ M, the frequency (f) of rhythmic contractions increases from 0.2 to 0.65 [sec<sup>–1</sup>], when the mean circumferential wall stress (σ) is increased from 1 · 10<sup>5</sup> to 1 · 10<sup>6</sup> dyn/cm<sup>2</sup>. The relationship between f and σ is, at a constant smooth muscle tone, virtually independent of the rate and also of the direction of the applied stress changes. Changes of the smooth muscle tone (i.e. changes of the actively developed wall stress), induced by vasoactive agents or other stimuli, lead to virtually parallel shifts of the σ-f relationship, which is obtained by passive stretching. It is concluded that the actual stimulus for the stretch-sensing structure in the arterial smooth muscle is the change in wall stress rather than the change in strain. Since rhythmic contractions may still be observed 30–60 min after withdrawal of Ca<sup>++</sup> from the bath solution, extracellular Ca<sup>++</sup> seems not to be primarily involved in this rhythmicity.