Clapp L H, Gurney A M, Standen N B, Langton P D
Cardiovascular Research, Rayne Institute, St Thomas's Hospital, London, United Kingdom.
J Membr Biol. 1994 Jun;140(3):205-13. doi: 10.1007/BF00233709.
Tension and patch clamp recording techniques were used to investigate the relaxation of rabbit pulmonary artery and the properties of the K+ current activated by levcromakalim in isolated myocytes. Under whole-cell voltage clamp, holding at -60 mV in symmetrical 139 mM K+, levcromakalim (10 microM) induced a noisy inward current of -116 +/- 19 pA (n = 13) which developed over 1 to 2 min. This current could be blocked by either glibenclamide (10 microM) or phencyclidine (5-50 microM) and was unaffected when extracellular Ca2+ was removed. Both these drugs inhibited the levcromakalim-induced relaxation of muscle strips precontracted with 20 mM [K+]o. Application of voltage ramps in symmetrical 139 mM K+ confirmed that the levcromakalim-induced current was carried by K+ ions and was weakly voltage dependent over the potential range from -100 to +40 mV. The unitary current amplitude and density of the channels underlying the levcromakalim-activated whole-cell K+ current was estimated from the noise in the current record. We estimate that levcromakalim caused activation of around 300 channels per cell, with a single channel current of 1.1 pA, corresponding to a slope conductance of about 19 pS. Furthermore, cells dialyzed with an ATP-free pipette solution developed a large noisy inward current at -60 mV, which could subsequently be blocked by flash photolysis of caged ATP. Analysis of the noise associated with this current indicated that the single channel amplitude underlying the ATP-blocked current was 1.4 pA, a value similar to that estimated for the levcromakalim-induced current.(ABSTRACT TRUNCATED AT 250 WORDS)