Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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 microM), 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 microM), 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.

Type

Journal article

Journal

J Physiol

Publication Date

01/02/2002

Volume

538

Pages

867 - 878

Keywords

Animals, Elapid Venoms, Electric Conductivity, Electrophysiology, Male, Muscle, Smooth, Vascular, Neurotoxins, Potassium Channels, Voltage-Gated, Pulmonary Artery, Rats, Rats, Wistar, Vascular Resistance