The epithelial or endothelial cells that line the human bronchi and the aorta express nicotinic acetylcholine receptors (nAChRs) of α3 subtypes. We report here that human bronchial epithelial cells (BEC) and aortic endothelial cells (AEC) express also the nAChR α7 subunit, which forms functional nAChRs. Polymerase chain reaction and in situ hybridization experiments detected α7 subunit mRNA in cultured human BEC and AEC and in sections of rat trachea. The binding of radiolabeled α-bungarotoxin revealed a few thousand binding sites per cell in cultured human BEC and human and bovine AEC. Western blot and immunohistochemistry experiments demonstrated that cultured BEC and AEC express a protein(s) recognized by anti-α7 antibodies. Whole-cell patch-clamp studies of cultured human BEC demonstrated the presence of fast-desensitizing currents activated by choline and nicotine that were blocked reversibly by methyllycaconitine (1 nM) and irreversibly by α-bungarotoxin (100 nM), consistent with the expression of functional α7 nAChRs. In some cells, choline activated also slowly decaying currents, confirming previous reports that BEC express functional α3β4 nAChRs. Exposure of cultured BEC to nicotine (1 μM) for 3 days up-regulated functional α7 and α3 nAChRs, as indicated by the increased number of cells responding to acetylcholine and choline, with both fast-desensitizing currents, which were blocked irreversibly by α-bungarotoxin, and with slowly desensitizing currents, which are α-bungarotoxin–insensitive currents. The presence of α7 nAChRs in BEC and AEC suggests that some toxic effects of tobacco smoke could be mediated through these nicotine-sensitive receptors.