The endothelial and the vascular smooth muscle cells of an arterial strip of coronary artery of the pig are not dye-coupled. However, substance P and bradykinin induce an hyperpolarization of the endothelial cells and, simultaneously, an endothelium-dependent relaxation and hyperpolarization of the smooth muscle cells. Therefore the question arises about a possible causality between these two hyperpolarizations. To answer this question, the hypothesis that the endothelial cells are coupled electrically by gap junctions to the underlying smooth muscle cells was tested by observing whether or not changes in membrane potentials that occur in the smooth muscle cells would be transmitted to the endothelial cells. Hyperpolarization caused to smooth muscle cells by a beta-adrenergic agonist, and action potentials generated in these cells by a blocker of potassium channels were transmitted to the adjoining endothelial cells. These observations suggest a heterologous cell electrical coupling. Halothane, a molecule known to uncouple cells linked by gap junctions, inhibited the transmission of electrical signals from the smooth muscle to the endothelial cells, but did not inhibit the propagation of hyperpolarization caused by substance P and bradykinin from the endothelium to the smooth muscle cells. These observations suggest the existence of an asymetric barrier to the movement of ions by heterologous coupling in the arterial wall. They strengthen the concept that endothelium-dependent hyperpolarizing factor is a chemical messenger. It remains to explain how a paracrine factor can faithfully reproduce in the smooth muscle cells hyperpolarizations that are generated in the endothelium in response to kinins.