The patch-clamp technique was used to study the electrophysiological properties of single smooth muscle cells obtained from the human cystic artery. These cells contracted on exposure to high K+and had a mean resting potential of −36±7 mV. Under current clamp, regenerative responses could not be elicited when depolarizing pulses were applied. Voltage-clamp measurements demonstrated that a large fraction of the outward current was inhibited by tetraethylammonium (5–10 mM) or Ca2+channel blockers and that it was enhanced by increasing [Ca2+], suggesting that it is a Ca2+-activated K+current. In addition, spontaneous transient outward currents that were sensitive to extracellular Ca2+were observed in some cells. In cell-attached patch-clamp recordings, Ca2+-activated K+channels that had a conductance of 117 pS were consistently identified. At negative potentials (approximately −60 mV), these single-channel events deactivated completely and very quickly, suggesting that they do not control the resting membrane potential in healthy cystic artery cells. Ca2+currents that were recorded using Ba2+(10 mM) as the charge carrier were enhanced by the dihydropyridine agonist, Bay K 8644, and blocked by nifedipine (0.1 μM). Only one type of Ca2+current, the L-type, could be identified in these cells. These results demonstrate that the major ionic currents in the human cystic artery are similar to other mammalian arteries and indicate that this tissue will be a useful model for studying the metabolic and pharmacological modulation of ionic currents in human vascular smooth muscle. (Circulation Research1992;70:536–545)