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Pulmonary arteries (PAs), particularly those of the rat, demonstrate a prominent voltage-gated K+ (Kv) current (Ikv), which plays an important role in the regulation of the resting potential. No detailed characterization of electrophysiological and pharmacological properties of Ikv, particularly in resistance PA myocytes (PAMs), has been performed. The aim of the present study was therefore to compare Ikv in rat conduit and resistance PAMs using the standard patch clamp technique. We found that 67 % of conduit PAMs demonstrated a large, rapidly activating Ikv which was potently blocked by 4-aminopyridine (4-AP; IC50, 232 μm), but was almost insensitive to TEA (18 % block at 20 mm). Thirty-three percent of cells exhibited a smaller, more slowly activating Ikv which was TEA sensitive (IC50, 2.6 mm) but relatively insensitive to 4-AP (37 % block at 20 mm). These currents (termed Ikv1 and Ikv2, respectively) inactivated over different ranges of potential (V0.5 =−20.2 vs. -39.1 mV, respectively). All resistance PAMs demonstrated a large, rapidly activating and TEA-insensitive K+ current resembling Ikv1 (termed Ikvr), but differing significantly from it with respect to 4-AP sensitivity (IC50, 352 μm), activation rate, and inactivation potential range (V0.5, −27.4 mV). Thus, cells from conduit PAMs fall into two populations with respect to functional Ikv expression, while resistance arteries uniformly demonstrate a third type of Ikv. Comparison of the properties of the native Ikv with those of cloned Kv channel currents suggest that Ikv1 and Ikvr are likely to be mediated by Kv1.5-containing homo/heteromultimers, while Ikv2 involves a Kv2.1 α-subunit.

Original publication




Journal article


The Journal of Physiology

Publication Date





867 - 878