Electrophysiologically distinct smooth muscle cell subtypes in rat conduit and resistance pulmonary arteries

Pulmonary arteries (PAs), particularly those of the rat, demonstrate a prominent voltage‐gated K + (Kv) current ( I k v ), which plays an important role in the regulation of the resting potential. No detailed characterization of electrophysiological and pharmacological properties of I k v , particularly in resistance PA myocytes (PAMs), has been performed. The aim of the present study was therefore to compare I k v in rat conduit and resistance PAMs using the standard patch clamp technique. We found that 67 % of conduit PAMs demonstrated a large, rapidly activating I k v which was potently blocked by 4‐aminopyridine (4‐AP; IC 50 , 232 μ m ), but was almost insensitive to TEA (18 % block at 20 m m ). Thirty‐three percent of cells exhibited a smaller, more slowly activating I k v which was TEA sensitive (IC 50 , 2.6 m m ) but relatively insensitive to 4‐AP (37 % block at 20 m m ). These currents (termed I k v1 and I k v2 , respectively) inactivated over different ranges of potential ( V 0.5 =−20.2 vs. ‐ 39.1 mV, respectively). All resistance PAMs demonstrated a large, rapidly activating and TEA‐insensitive K + current resembling I k v1 (termed I k v r ), but differing significantly from it with respect to 4‐AP sensitivity (IC 50 , 352 μ m ), activation rate, and inactivation potential range ( V 0.5 , −27.4 mV). Thus, cells from conduit PAMs fall into two populations with respect to functional I k v expression, while resistance arteries uniformly demonstrate a third type of I k v . Comparison of the properties of the native I k v with those of cloned Kv channel currents suggest that I k v1 and I k v r are likely to be mediated by Kv1.5‐containing homo/heteromultimers, while I k v2 involves a Kv2.1 α‐subunit.