Using strips of the left descending branch of the pig coronary artery in vitro, we show that smooth muscle cells are hyperpolarized by isoproterenol, a beta-agonist, independently of the presence or absence of intact endothelium. This hyperpolarization is transmitted to the lining endothelial cells in intact coronary strips. On the contrary, the cultured endothelial cells, without contact with smooth muscles, are not hyperpolarized by the beta-agonist. This shows that, in addition to the hyperpolarizations that flow from the endothelium to the media in response to kinins, electrical signals are also transmitted in the opposite direction, from the smooth muscles to the lining endothelial cells. In an attempt to test whether electrical coupling through gap junctions is implicated in the transmission of hyperpolarizations between the endothelial and the smooth muscle cells, we used halothane, a gap junction uncoupler. We observed that halothane does not inhibit the transmission of kinin hyperpolarizations from the endothelium to the smooth muscles, whereas it inhibits the transmission of isoproterenol hyperpolarization in the reverse direction.