Activation of inward rectifier K+ channels by hypoxia in rabbit coronary arterial smooth muscle cells
- Authors
- Park, Won Sun; Han, Jin; Kim, Nari; Ko, Jae-Hong; Kim, Sung Joon; Earm, Yung E
- Issue Date
- Dec-2005
- Publisher
- American Physiological Society
- Keywords
- inwardly rectifying K+ currentcoronary vasodilationprotein kinase AKir2.1
- Citation
- American Journal of Physiology - Heart and Circulatory Physiology, v.289, no.6, pp H2461 - H2467
- Journal Title
- American Journal of Physiology - Heart and Circulatory Physiology
- Volume
- 289
- Number
- 6
- Start Page
- H2461
- End Page
- H2467
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/66784
- DOI
- 10.1152/ajpheart.00331.2005
- ISSN
- 0363-6135
1522-1539
- Abstract
- We examined the effects of acute hypoxia on Ba2+-sensitive inward rectifier K+ (KIR) current in rabbit coronary arterial smooth muscle cells. The amplitudes of KIR current was definitely higher in the cells from small-diameter (<100 μm) coronary arterial smooth muscle cells (SCASMC, -12.8 ± 1.3 pA/pF at -140 mV) than those in large-diameter coronary arterial smooth muscle cells (>200 μm, LCASMC, -1.5 ± 0.1 pA pF-1). Western blot analysis confirmed that Kir2.1 protein was expressed in SCASMC but not LCASMC. Hypoxia activated much more KIR currents in symmetrical 140 K+. This effect was blocked by the adenylyl cyclase inhibitor SQ-22536 (10 μM) and mimicked by forskolin (10 μM) and dibutyryl-cAMP (500 μM). The production of cAMP in SCASMC increased 5.7-fold after 6 min of hypoxia. Hypoxia-induced increase in KIR currents was abolished by the PKA inhibitors, Rp-8-(4-chlorophenylthio)-cAMPs (10 μM) and KT-5720 (1 μM). The inhibition of G protein with GDPβS (1 mM) partially reduced (∼50%) the hypoxia-induced increase in KIR currents. In Langendorff-perfused rabbit hearts, hypoxia increased coronary blood flow, an effect that was inhibited by Ba2+. In summary, hypoxia augments the KIR currents in SCASMC via cAMP- and PKA-dependent signaling cascades, which might, at least partly, explain the hypoxia-induced coronary vasodilation. Copyright © 2005 the American Physiological Society.
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