Oscillatory contractions of arteries in vitro are frequently induced by receptor stimulation with agonists. In certain arteries, the membrane potential and cytoplasmic intracellular free Ca²⁺ concentration in smooth muscle cells oscillate in the presence of agonists. The oscillatory changes are related to the Ca²⁺ release from store sites as well as Ca²⁺ influx. Gap junctions between smooth muscle cells play important roles in the synchronization of Ca²⁺ concentration in arterial tissues. Some of the agonist-induced oscillatory contractions are dependent on endothelium. Endothelial cells or endothelium-derived substances may modulate the tension oscillation of smooth muscle cells. In arteries from hypertensive animals, oscillatory contraction has been induced by agonists more frequently than that from normotensive animals. Abnormalities in membrane excitability of smooth muscle cells, gap junctions and endothelium may influence the tension oscillation in arteries from hypertensive rats.

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