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

S V Smirnov, R Beck, P Tammaro, T Ishii, P I Aaronson

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    58 Citations (Scopus)

    Abstract

    Pulmonary arteries (PAs), particularly those of the rat, demonstrate a prominent voltage-gated K+ (Kv) current (I-Kv), which plays an important role in the regulation of the resting potential. No detailed characterization of electrophysiological and pharmacological properties of I-Kv, particularly in resistance PA myocytes (PAMs), has been performed. The aim of the present study was therefore to compare I-Kv 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-Kv which was potently blocked by 4-aminopyridine (4-AP; IC50, 232 muM), but was almost insensitive to TEA (18 % block at 20 mm). Thirty-three percent of cells exhibited a smaller, more slowly activating I-Kv which was TEA sensitive (IC50, 2.6 mM) but relatively insensitive to 4-AP (37 % block at 20 mm). These currents (termed I-Kv1 and I-Kv2, 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-Kv1 (termed I-KvR), but differing significantly from it with respect to 4-AP sensitivity (IC50, 352 muM), 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-Kv expression, while resistance arteries uniformly demonstrate a third type of I-Kv. Comparison of the properties of the native I-Kv with those of cloned Kv channel currents suggest that I-Kv1 and I-KvR are likely to be mediated by Kv1.5-containing homo/heteromultimers, while I-Kv2 involves a Kv2.1 alpha-subunit.
    Original languageEnglish
    Pages (from-to)867 - 878
    Number of pages12
    JournalThe Journal of Physiology
    Volume538
    Issue number3
    DOIs
    Publication statusPublished - 1 Feb 2002

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