Hypoxia sensitivity of a voltage-gated potassium current in porcine intrapulmonary vein smooth muscle cells

C. Dospinescu, H. Widmer, I. Rowe, C. Wainwright, S.F. Cruickshank

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8 Citations (Scopus)


Hypoxia contracts the pulmonary vein, but the underlying cellular effectors remain unclear. Utilizing contractile studies and whole cell patch-clamp electrophysiology, we report for the first time a hypoxia-sensitive K+ current in porcine pulmonary vein smooth muscle cells (PVSMC). Hypoxia induced a transient contractile response that was 56 ± 7% of the control response (80 mM KCl). This contraction required extracellular Ca2+ and was sensitive to Ca2+ channel blockade. Blockade of K+ channels by tetraethylammonium chloride (TEA) or 4-aminopyridine (4-AP) reversibly inhibited the hypoxia-mediated contraction. Single-isolated PVSMC (typically 159.1 ± 2.3 μm long) had mean resting membrane potentials (RMP) of −36 ± 4 mV with a mean membrane capacitance of 108 ± 3.5 pF. Whole cell patch-clamp recordings identified a rapidly activating, partially inactivating K+ current (IKH) that was hypoxia, TEA, and 4-AP sensitive. IKH was insensitive to Penitrem A or glyburide in PVSMC and had a time to peak of 14.4 ± 3.3 ms and recovered in 67 ms following inactivation at +80 mV. Peak window current was −32 mV, suggesting that IKH may contribute to PVSMC RMP. The molecular identity of the potassium channel is not clear. However, RT-PCR, using porcine pulmonary artery and vein samples, identified Kv1.5, Kv2.1, and BK, with all three being more abundant in the PV. Both artery and vein expressed STREX, a highly conserved and hypoxia-sensitive BK channel variant. Taken together, our data support the hypothesis that hypoxic inhibition of IKH would contribute to hypoxic-induced contraction in PVSMC.
Original languageEnglish
Pages (from-to)10
Number of pages476
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Early online date6 Jul 2012
Publication statusPublished - 1 Sept 2012

Bibliographical note

Present address for Dr.Ciprian Dospinescu: Department of Cardiology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB25 2ZN, Scotland.
This work was supported by the Overseas Research Students Awards Scheme, The Ratiu Foundation UK, Robert Gordon University Research Development Initiative, and Tenovus Scotland (Grant no. GO4.9).
No conflicts of interest, financial or otherwise are declared by the author(s).


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