Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes
Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic...
Uložené v:
| Vydané v: | The Journal of clinical investigation Ročník 101; číslo 11; s. 2319 |
|---|---|
| Hlavní autori: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
01.06.1998
|
| Predmet: | |
| ISSN: | 0021-9738 |
| On-line prístup: | Zistit podrobnosti o prístupe |
| Tagy: |
Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
|
| Abstract | Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families of Kv channels known and pharmacological inhibitors lack the specificity to distinguish those involved in control of resting membrane potential (Em) or HPV. However, the Kv channels involved in Em and HPV have characteristic electrophysiological and pharmacological properties which suggest their molecular identity. They are slowly inactivating, delayed rectifier currents, inhibited by 4-aminopyridine (4-AP) but insensitive to charybdotoxin. Candidate Kv channels with these traits (Kv1.5 and Kv2.1) were studied. Antibodies were used to immunolocalize and functionally characterize the contribution of Kv1. 5 and Kv2.1 to PASMC electrophysiology and vascular tone. Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs. Intracellular administration of anti-Kv2.1 inhibited whole cell K+ current (IK) and depolarized Em. Anti-Kv2.1 also elevated resting tension and diminished 4-AP-induced vasoconstriction in membrane-permeabilized pulmonary artery rings. Anti-Kv1.5 inhibited IK and selectively reduced the rise in [Ca2+]i and constriction caused by hypoxia and 4-AP. However, anti-Kv1.5 neither caused depolarization nor elevated basal pulmonary artery tone. This study demonstrates that antibodies can be used to dissect the whole cell K+ currents in mammalian cells. We conclude that Kv2. 1 is an important determinant of resting Em in PASMCs from resistance arteries. Both Kv2.1 and Kv1.5 contribute to the initiation of HPV. |
|---|---|
| AbstractList | Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families of Kv channels known and pharmacological inhibitors lack the specificity to distinguish those involved in control of resting membrane potential (Em) or HPV. However, the Kv channels involved in Em and HPV have characteristic electrophysiological and pharmacological properties which suggest their molecular identity. They are slowly inactivating, delayed rectifier currents, inhibited by 4-aminopyridine (4-AP) but insensitive to charybdotoxin. Candidate Kv channels with these traits (Kv1.5 and Kv2.1) were studied. Antibodies were used to immunolocalize and functionally characterize the contribution of Kv1. 5 and Kv2.1 to PASMC electrophysiology and vascular tone. Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs. Intracellular administration of anti-Kv2.1 inhibited whole cell K+ current (IK) and depolarized Em. Anti-Kv2.1 also elevated resting tension and diminished 4-AP-induced vasoconstriction in membrane-permeabilized pulmonary artery rings. Anti-Kv1.5 inhibited IK and selectively reduced the rise in [Ca2+]i and constriction caused by hypoxia and 4-AP. However, anti-Kv1.5 neither caused depolarization nor elevated basal pulmonary artery tone. This study demonstrates that antibodies can be used to dissect the whole cell K+ currents in mammalian cells. We conclude that Kv2. 1 is an important determinant of resting Em in PASMCs from resistance arteries. Both Kv2.1 and Kv1.5 contribute to the initiation of HPV. Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families of Kv channels known and pharmacological inhibitors lack the specificity to distinguish those involved in control of resting membrane potential (Em) or HPV. However, the Kv channels involved in Em and HPV have characteristic electrophysiological and pharmacological properties which suggest their molecular identity. They are slowly inactivating, delayed rectifier currents, inhibited by 4-aminopyridine (4-AP) but insensitive to charybdotoxin. Candidate Kv channels with these traits (Kv1.5 and Kv2.1) were studied. Antibodies were used to immunolocalize and functionally characterize the contribution of Kv1. 5 and Kv2.1 to PASMC electrophysiology and vascular tone. Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs. Intracellular administration of anti-Kv2.1 inhibited whole cell K+ current (IK) and depolarized Em. Anti-Kv2.1 also elevated resting tension and diminished 4-AP-induced vasoconstriction in membrane-permeabilized pulmonary artery rings. Anti-Kv1.5 inhibited IK and selectively reduced the rise in [Ca2+]i and constriction caused by hypoxia and 4-AP. However, anti-Kv1.5 neither caused depolarization nor elevated basal pulmonary artery tone. This study demonstrates that antibodies can be used to dissect the whole cell K+ currents in mammalian cells. We conclude that Kv2. 1 is an important determinant of resting Em in PASMCs from resistance arteries. Both Kv2.1 and Kv1.5 contribute to the initiation of HPV.Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families of Kv channels known and pharmacological inhibitors lack the specificity to distinguish those involved in control of resting membrane potential (Em) or HPV. However, the Kv channels involved in Em and HPV have characteristic electrophysiological and pharmacological properties which suggest their molecular identity. They are slowly inactivating, delayed rectifier currents, inhibited by 4-aminopyridine (4-AP) but insensitive to charybdotoxin. Candidate Kv channels with these traits (Kv1.5 and Kv2.1) were studied. Antibodies were used to immunolocalize and functionally characterize the contribution of Kv1. 5 and Kv2.1 to PASMC electrophysiology and vascular tone. Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs. Intracellular administration of anti-Kv2.1 inhibited whole cell K+ current (IK) and depolarized Em. Anti-Kv2.1 also elevated resting tension and diminished 4-AP-induced vasoconstriction in membrane-permeabilized pulmonary artery rings. Anti-Kv1.5 inhibited IK and selectively reduced the rise in [Ca2+]i and constriction caused by hypoxia and 4-AP. However, anti-Kv1.5 neither caused depolarization nor elevated basal pulmonary artery tone. This study demonstrates that antibodies can be used to dissect the whole cell K+ currents in mammalian cells. We conclude that Kv2. 1 is an important determinant of resting Em in PASMCs from resistance arteries. Both Kv2.1 and Kv1.5 contribute to the initiation of HPV. |
| Author | Souil, E Dinh-Xuan, A T Mercier, J C El Yaagoubi, A Archer, S L Nguyen-Huu, L Schremmer, B Reeve, H L Hampl, V |
| Author_xml | – sequence: 1 givenname: S L surname: Archer fullname: Archer, S L organization: Veteran's Affairs Medical Center, Minneapolis, Minnesota 55417 and University of Alberta, Edmonton, Alberta, Canada – sequence: 2 givenname: E surname: Souil fullname: Souil, E – sequence: 3 givenname: A T surname: Dinh-Xuan fullname: Dinh-Xuan, A T – sequence: 4 givenname: B surname: Schremmer fullname: Schremmer, B – sequence: 5 givenname: J C surname: Mercier fullname: Mercier, J C – sequence: 6 givenname: A surname: El Yaagoubi fullname: El Yaagoubi, A – sequence: 7 givenname: L surname: Nguyen-Huu fullname: Nguyen-Huu, L – sequence: 8 givenname: H L surname: Reeve fullname: Reeve, H L – sequence: 9 givenname: V surname: Hampl fullname: Hampl, V |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/9616203$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNUE1P3DAQ9QFEgbb_oJJPXCBbe-JNNkeEyocA9QLn1cSZ7Bo5dmo7K_b_9YfVoXvg9EZv3rz3NGfsyHlHjH2XYiFlDT_ftCnL8oidCgGyaOpy9YWdxfgmhFRqqU7YSVPJCkR5yv4-e0t6shi46cgl0xuNyXjHfc_TlnjI-3neeZtwQ8UGE3X88ZLrLTpHNl7xx51cLDm6TO9gIa-4cXy7H_270Xyc7OAdhj3fYfTau5iC0R8B80EmUk6YAwLFZNyGDzS0AR3x0ae5ENrZL2D65IUhUYZh7_U-UfzKjnu0kb4d8Jy93v56ubkvnn7fPdxcPxVaQZUK6GQlkTrVtSvV9bLtpYSmVbWo2woUVVCutFBEqkOCZQlQQd9L0nWjRI0I5-ziv-8Y_J8p910PJmqyNtf1U1zXTQMlKMjCHwfh1A7Urcdghtx7fXg7_AMThYby |
| CitedBy_id | crossref_primary_10_1096_fj_99_0859com crossref_primary_10_1111_j_1476_5381_2009_00283_x crossref_primary_10_1161_CIRCRESAHA_109_206334 crossref_primary_10_1152_physrev_00030_2011 crossref_primary_10_1016_j_mod_2017_06_001 crossref_primary_10_1113_jphysiol_2008_165217 crossref_primary_10_1086_675980 crossref_primary_10_1183_13993003_00754_2017 crossref_primary_10_1016_j_resp_2010_08_007 crossref_primary_10_1016_j_athoracsur_2003_11_035 crossref_primary_10_3389_fcvm_2023_1125063 crossref_primary_10_1165_rcmb_2013_0191OC crossref_primary_10_3390_ijms26146857 crossref_primary_10_1113_jphysiol_2003_058594 crossref_primary_10_1016_j_bbrc_2007_05_102 crossref_primary_10_1016_j_pbiomolbio_2009_10_001 crossref_primary_10_1080_10739680600930313 crossref_primary_10_1089_ars_2009_2862 crossref_primary_10_1038_sj_bjp_0706285 crossref_primary_10_1016_j_abb_2019_108234 crossref_primary_10_1152_japplphysiol_00722_2004 crossref_primary_10_1002_j_2040_4603_2020_tb00125_x crossref_primary_10_1016_j_pharmthera_2007_03_014 crossref_primary_10_1111_bph_12822 crossref_primary_10_1161_01_CIR_101_8_923 crossref_primary_10_1016_j_ceca_2004_02_018 crossref_primary_10_1016_j_freeradbiomed_2019_04_008 crossref_primary_10_1016_j_ceca_2004_02_017 crossref_primary_10_1161_CIRCRESAHA_118_314284 crossref_primary_10_3892_ol_2012_718 crossref_primary_10_1113_jphysiol_2002_025171 crossref_primary_10_1196_annals_1378_053 crossref_primary_10_1111_j_1742_7843_2011_00855_x crossref_primary_10_1016_j_neuroscience_2003_08_036 crossref_primary_10_1085_jgp_201511507 crossref_primary_10_1152_physrev_00032_2009 crossref_primary_10_1016_S1537_1891_02_00126_X crossref_primary_10_1016_j_bbabio_2012_12_002 crossref_primary_10_1023_B_NEPH_0000008784_83366_9a crossref_primary_10_1016_j_chest_2016_09_001 crossref_primary_10_1161_01_CIR_0000062688_76508_B3 crossref_primary_10_1016_j_yjmcc_2010_09_012 crossref_primary_10_1113_JP272032 crossref_primary_10_1523_JNEUROSCI_19_05_01728_1999 crossref_primary_10_1016_j_freeradbiomed_2011_12_004 crossref_primary_10_1016_S1569_9048_02_00054_X crossref_primary_10_1086_674307 crossref_primary_10_3389_fphys_2018_00865 crossref_primary_10_3389_fphys_2020_00947 crossref_primary_10_1016_S0034_5687_99_00025_0 crossref_primary_10_1161_CIRCRESAHA_111_247940 crossref_primary_10_1203_PDR_0b013e3181b1bc89 crossref_primary_10_1111_j_1469_7793_2000_00783_x crossref_primary_10_1016_j_jneumeth_2005_04_015 crossref_primary_10_1016_j_resp_2010_08_013 crossref_primary_10_1016_j_omtn_2020_09_029 crossref_primary_10_1038_s41572_023_00486_7 crossref_primary_10_3390_biom10091261 crossref_primary_10_1517_14728222_2016_1112792 crossref_primary_10_1080_10739680600930222 crossref_primary_10_1097_MJT_0b013e318249a08c crossref_primary_10_1111_j_1748_1716_2008_01894_x crossref_primary_10_1161_01_RES_0000137173_42723_fb crossref_primary_10_1113_jphysiol_2001_013003 crossref_primary_10_1164_rccm_200711_1631OC crossref_primary_10_1016_j_bbrc_2006_06_116 crossref_primary_10_4331_wjbc_v5_i2_85 crossref_primary_10_1016_j_pcl_2009_04_004 crossref_primary_10_1161_hc0202_101974 crossref_primary_10_1586_ecp_10_18 crossref_primary_10_1152_japplphysiol_00929_2003 crossref_primary_10_1016_j_lfs_2015_12_054 crossref_primary_10_1113_jphysiol_2005_098855 crossref_primary_10_1097_00005392_200204000_00100 crossref_primary_10_1002_j_2040_4603_2011_tb00316_x crossref_primary_10_7554_eLife_90604 crossref_primary_10_1016_S0006_8993_01_02121_7 crossref_primary_10_1073_pnas_96_14_7944 crossref_primary_10_3390_biom12101341 crossref_primary_10_3389_fncel_2014_00329 crossref_primary_10_1124_jpet_108_138032 crossref_primary_10_1089_ars_2014_5899 crossref_primary_10_1161_hh2301_100817 crossref_primary_10_1161_01_RES_85_6_489 crossref_primary_10_1111_bph_16426 crossref_primary_10_1016_j_freeradbiomed_2019_09_029 crossref_primary_10_1152_physrev_00041_2010 crossref_primary_10_1016_S1537_1891_02_00127_1 crossref_primary_10_3389_fcell_2023_1105565 crossref_primary_10_1126_scitranslmed_3001327 crossref_primary_10_1186_ar4124 crossref_primary_10_1124_jpet_108_147785 crossref_primary_10_1161_CIRCRESAHA_115_301130 crossref_primary_10_1152_ajpheart_2001_281_3_H1057 crossref_primary_10_1371_journal_pone_0141349 crossref_primary_10_1073_pnas_1917879117 crossref_primary_10_1113_jphysiol_2007_128454 crossref_primary_10_1089_ars_2009_2877 crossref_primary_10_1016_j_placenta_2004_11_008 crossref_primary_10_1186_1465_9921_12_20 crossref_primary_10_1038_nrd2983 crossref_primary_10_1089_ham_2013_1016 crossref_primary_10_1183_09031936_04_00037204 crossref_primary_10_3389_fphys_2023_1142354 crossref_primary_10_1186_s12931_025_03163_3 crossref_primary_10_1515_BC_2004_014 crossref_primary_10_1111_j_1469_7793_2001_00691_x crossref_primary_10_1016_j_pbiomolbio_2007_07_007 crossref_primary_10_5387_fms_2014_34 crossref_primary_10_1139_y99_098 crossref_primary_10_1016_S0024_3205_00_00529_4 crossref_primary_10_1080_10641950701826158 crossref_primary_10_1016_j_cmet_2014_08_011 crossref_primary_10_1016_S1569_9048_02_00051_4 crossref_primary_10_1002_jcp_1069 crossref_primary_10_1152_japplphysiol_00103_2017 crossref_primary_10_1002_j_1939_4640_2002_tb02348_x crossref_primary_10_1161_01_RES_86_5_534 crossref_primary_10_1016_j_abb_2019_01_029 crossref_primary_10_1016_j_ejphar_2003_10_028 crossref_primary_10_1016_S0026_895X_24_23177_1 crossref_primary_10_1161_01_RES_0000035057_63303_D1 crossref_primary_10_1016_S0140_6736_00_02452_1 crossref_primary_10_3390_biology12091237 crossref_primary_10_1016_S0008_6363_02_00411_X crossref_primary_10_1016_j_bbabio_2022_148911 crossref_primary_10_1016_S0022_5347_05_65254_8 crossref_primary_10_1186_rr11 crossref_primary_10_1161_01_CIR_102_22_2781 crossref_primary_10_1152_ajplung_2001_281_5_L1115 crossref_primary_10_1016_j_vph_2008_07_006 crossref_primary_10_1291_hypres_25_589 crossref_primary_10_1016_j_cjca_2014_10_023 crossref_primary_10_1152_jappl_2001_90_6_2249 crossref_primary_10_1161_HYPERTENSIONAHA_114_03406 crossref_primary_10_1183_09031936_01_17100200 crossref_primary_10_3390_ijms19103162 crossref_primary_10_1371_journal_pone_0086636 crossref_primary_10_1152_japplphysiol_00843_2012 crossref_primary_10_1016_S1569_9048_02_00047_2 crossref_primary_10_1172_JCI59176 crossref_primary_10_1152_japplphysiol_01110_2001 crossref_primary_10_1146_annurev_physiol_030212_183804 crossref_primary_10_1016_j_lfs_2004_10_073 crossref_primary_10_1016_j_freeradbiomed_2020_12_452 crossref_primary_10_1016_j_drudis_2024_104015 crossref_primary_10_1161_CIRCRESAHA_111_263848 crossref_primary_10_1016_S1537_1891_02_00121_0 crossref_primary_10_1177_1753465808091327 crossref_primary_10_1152_ajplung_2001_281_6_L1350 crossref_primary_10_1183_09031936_02_00081302 crossref_primary_10_3389_fphys_2017_00903 crossref_primary_10_1074_jbc_RA118_004065 crossref_primary_10_1152_ajplung_2001_280_6_L1138 crossref_primary_10_1161_hh1201_091960 crossref_primary_10_1016_j_pharmthera_2014_08_001 crossref_primary_10_1161_01_ATV_0000158497_09626_3b crossref_primary_10_1097_00000441_200104000_00009 crossref_primary_10_1165_rcmb_2003_0386OC crossref_primary_10_1016_S0163_7258_02_00201_2 crossref_primary_10_1038_sj_bjp_0707635 crossref_primary_10_1016_j_yjmcc_2006_03_431 crossref_primary_10_1080_10409238_2021_2004575 crossref_primary_10_1086_689748 crossref_primary_10_1152_ajpheart_01033_2001 crossref_primary_10_1053_pcad_2002_127491 crossref_primary_10_1113_JP282231 crossref_primary_10_1016_S0764_4469_00_86653_6 crossref_primary_10_1152_ajplung_2001_281_6_L1345 crossref_primary_10_1183_09031936_00013908 crossref_primary_10_1007_s11062_005_0021_7 crossref_primary_10_1089_ars_2012_4752 crossref_primary_10_1161_01_RES_0000247068_75808_3f crossref_primary_10_1016_j_bbrc_2005_08_180 crossref_primary_10_1016_S0022_3565_24_29480_5 crossref_primary_10_1089_ars_2014_6234 crossref_primary_10_1161_CIRCULATIONAHA_111_034512 crossref_primary_10_1016_j_jacc_2009_04_014 crossref_primary_10_1016_j_resp_2005_10_003 crossref_primary_10_1183_09031936_01_00204001 crossref_primary_10_1016_S1537_1891_02_00122_2 crossref_primary_10_1086_680189 crossref_primary_10_1161_JAHA_117_006465 crossref_primary_10_1113_jphysiol_2013_257253 crossref_primary_10_1152_ajplung_2001_281_1_L1 crossref_primary_10_1183_13993003_00945_2015 crossref_primary_10_1016_j_lfs_2010_03_011 crossref_primary_10_1002_j_2040_4603_2011_tb00358_x crossref_primary_10_1161_01_RES_0000036751_04896_F1 crossref_primary_10_1016_j_ejphar_2014_11_007 crossref_primary_10_1161_01_RES_0000095245_97945_FE crossref_primary_10_1161_01_RES_0000145360_16770_9f crossref_primary_10_21693_1933_088X_3_3_6 crossref_primary_10_1016_j_resp_2014_09_025 crossref_primary_10_7554_eLife_90604_3 crossref_primary_10_1016_S0306_3623_99_00026_9 crossref_primary_10_1016_j_abb_2009_05_015 crossref_primary_10_1016_j_hlc_2023_01_013 crossref_primary_10_1038_cddis_2017_568 crossref_primary_10_1152_japplphysiol_00733_2004 crossref_primary_10_1152_ajplung_00238_2014 crossref_primary_10_1152_japplphysiol_00120_2017 crossref_primary_10_1161_01_RES_0000216858_04599_e1 crossref_primary_10_3390_biom12020265 crossref_primary_10_1016_j_placenta_2005_10_006 crossref_primary_10_1152_ajpcell_00967_2024 crossref_primary_10_1007_s00109_011_0762_2 crossref_primary_10_1016_S0272_5231_05_70281_1 crossref_primary_10_1096_fj_00_0649fje crossref_primary_10_4103_2045_8932_114776 crossref_primary_10_1111_j_1749_6632_2009_05040_x crossref_primary_10_1152_ajplung_1999_277_3_L431 crossref_primary_10_1161_01_RES_0000222546_45372_a0 crossref_primary_10_1016_j_bcp_2003_08_041 crossref_primary_10_1113_jphysiol_2004_073338 crossref_primary_10_1016_j_cellsig_2005_05_025 crossref_primary_10_1124_mol_107_037002 crossref_primary_10_1016_j_lfs_2005_10_042 crossref_primary_10_1111_j_1476_5381_2009_00353_x crossref_primary_10_1152_ajpgi_1999_277_5_G1055 crossref_primary_10_1016_S0024_3205_02_01922_7 crossref_primary_10_1111_j_1440_1843_2003_00531_x crossref_primary_10_1186_s13036_019_0221_0 crossref_primary_10_1093_cvr_cvq305 crossref_primary_10_1111_bph_14662 crossref_primary_10_1164_rccm_201508_1678OC crossref_primary_10_1074_jbc_RA119_011302 crossref_primary_10_1016_S0006_291X_02_02990_X |
| ContentType | Journal Article |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1172/jci333 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Medicine |
| ExternalDocumentID | 9616203 |
| Genre | Journal Article |
| GroupedDBID | --- -~X .55 .GJ .XZ 08P 29K 2WC 354 3O- 53G 5GY 5RE 5RS 8F7 AAWTL AAYOK ABOCM ABPMR ACGFO ACIHN ACNCT ACPRK ADBBV AEAQA AENEX AFCHL AFFNX AHMBA AI. ALIPV ALMA_UNASSIGNED_HOLDINGS AOIJS ASPBG AVWKF AZFZN BAWUL CGR CS3 CUY CVF D-I DIK DU5 E3Z EBS ECM EIF EJD EMB F5P FRP GROUPED_DOAJ GX1 HYE H~9 IAO IEA IHR INH INR IOF IPO J5H KQ8 L7B M1P M5~ MVM N4W NPM OBH OCB ODZKP OFXIZ OGEVE OHH OK1 OVD OVIDX P2P P6G PKN RPM TEORI TR2 TVE UHU VH1 VVN W2D WH7 WOQ WOW X7M XSB YFH YHG YKV YOC ZGI ZXP ZY1 ~H1 7X8 OVT |
| ID | FETCH-LOGICAL-c426t-2d161aed4db84df1bf1129b4707b624e6238c04ee4dae2532262ff1ec79407aa2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 341 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000074165900004&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 0021-9738 |
| IngestDate | Fri Sep 05 12:15:01 EDT 2025 Wed Feb 19 01:18:56 EST 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 11 |
| Language | English |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c426t-2d161aed4db84df1bf1129b4707b624e6238c04ee4dae2532262ff1ec79407aa2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | http://www.jci.org/articles/view/333/files/pdf |
| PMID | 9616203 |
| PQID | 79923242 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_79923242 pubmed_primary_9616203 |
| PublicationCentury | 1900 |
| PublicationDate | 1998-Jun-01 19980601 |
| PublicationDateYYYYMMDD | 1998-06-01 |
| PublicationDate_xml | – month: 06 year: 1998 text: 1998-Jun-01 day: 01 |
| PublicationDecade | 1990 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | The Journal of clinical investigation |
| PublicationTitleAlternate | J Clin Invest |
| PublicationYear | 1998 |
| References | 9362476 - EMBO J. 1997 Nov 17;16(22):6615-25 9005448 - Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15119-23 7542182 - Circ Res. 1995 Aug;77(2):370-8 8662756 - J Biol Chem. 1996 May 31;271(22):13239-43 8083226 - J Biol Chem. 1994 Sep 16;269(37):23204-11 7491983 - Am J Physiol. 1995 Nov;269(5 Pt 1):L637-44 8352944 - Neuron. 1993 Aug;11(2):359-69 7473178 - J Pharmacol Exp Ther. 1995 Nov;275(2):864-76 8524851 - Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11796-800 5914855 - Circ Res. 1966 Aug;19(2):426-40 1245025 - Circ Res. 1976 Feb;38(2):99-104 8279575 - Am J Physiol. 1993 Dec;265(6 Pt 1):L591-7 8204618 - Biochemistry. 1994 Jun 7;33(22):6834-9 8593702 - Circ Res. 1996 Mar;78(3):431-42 7623158 - J Neurosci. 1995 Jul;15(7 Pt 2):5360-71 7517498 - Mol Pharmacol. 1994 Jun;45(6):1227-34 8081723 - Receptors Channels. 1993;1(2):99-110 8447425 - Am J Physiol. 1993 Feb;264(2 Pt 1):L116-23 8903313 - J Clin Invest. 1996 Nov 1;98(9):1959-65 8901674 - Circulation. 1996 Nov 1;94(9):2216-20 8122319 - Trends Pharmacol Sci. 1993 Dec;14(12):434 8371757 - Nature. 1993 Sep 9;365(6442):153-5 9410914 - J Clin Invest. 1997 Nov 1;100(9):2347-53 2456613 - Science. 1988 Jul 29;241(4865):580-2 7977686 - Am J Physiol. 1994 Nov;267(5 Pt 1):C1231-8 9113366 - Br J Pharmacol. 1997 Apr;120(8):1461-70 7517960 - J Clin Pathol. 1994 May;47(5):448-52 8508921 - FEBS Lett. 1993 Jun 14;324(2):205-10 8355805 - Nature. 1993 Aug 26;364(6440):802-6 8304521 - Am J Physiol. 1994 Jan;266(1 Pt 2):H365-70 8110763 - Biochemistry. 1994 Feb 22;33(7):1617-23 8158277 - J Neurosci. 1994 Apr;14(4):2408-17 1839781 - Brain Res. 1991 Nov 15;564(2):203-19 8011897 - Biophys J. 1994 Mar;66(3 Pt 1):667-73 7615797 - J Clin Invest. 1995 Jul;96(1):282-92 8222081 - Circ Res. 1993 Dec;73(6):1100-12 8964107 - Circulation. 1996 Jul 1;94(1):1-5 2532193 - J Appl Physiol (1985). 1989 Nov;67(5):1903-11 2036711 - Circ Res. 1991 Jun;68(6):1569-81 1566816 - Am J Physiol. 1992 Apr;262(4 Pt 1):C882-90 1875913 - Mol Pharmacol. 1991 Aug;40(2):299-307 9067300 - J Pharmacol Exp Ther. 1997 Mar;280(3):1170-5 8938716 - Neuropharmacology. 1996;35(7):851-65 1415563 - Am J Physiol. 1992 Sep;263(3 Pt 1):L384-93 8447424 - Am J Physiol. 1993 Feb;264(2 Pt 1):L107-15 7788871 - Circ Res. 1995 Jul;77(1):131-9 |
| References_xml | – reference: 9113366 - Br J Pharmacol. 1997 Apr;120(8):1461-70 – reference: 1875913 - Mol Pharmacol. 1991 Aug;40(2):299-307 – reference: 8447424 - Am J Physiol. 1993 Feb;264(2 Pt 1):L107-15 – reference: 8110763 - Biochemistry. 1994 Feb 22;33(7):1617-23 – reference: 1839781 - Brain Res. 1991 Nov 15;564(2):203-19 – reference: 8083226 - J Biol Chem. 1994 Sep 16;269(37):23204-11 – reference: 9005448 - Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15119-23 – reference: 9067300 - J Pharmacol Exp Ther. 1997 Mar;280(3):1170-5 – reference: 8011897 - Biophys J. 1994 Mar;66(3 Pt 1):667-73 – reference: 8352944 - Neuron. 1993 Aug;11(2):359-69 – reference: 8355805 - Nature. 1993 Aug 26;364(6440):802-6 – reference: 1566816 - Am J Physiol. 1992 Apr;262(4 Pt 1):C882-90 – reference: 8903313 - J Clin Invest. 1996 Nov 1;98(9):1959-65 – reference: 2532193 - J Appl Physiol (1985). 1989 Nov;67(5):1903-11 – reference: 7542182 - Circ Res. 1995 Aug;77(2):370-8 – reference: 8371757 - Nature. 1993 Sep 9;365(6442):153-5 – reference: 5914855 - Circ Res. 1966 Aug;19(2):426-40 – reference: 7517498 - Mol Pharmacol. 1994 Jun;45(6):1227-34 – reference: 2456613 - Science. 1988 Jul 29;241(4865):580-2 – reference: 1415563 - Am J Physiol. 1992 Sep;263(3 Pt 1):L384-93 – reference: 2036711 - Circ Res. 1991 Jun;68(6):1569-81 – reference: 8122319 - Trends Pharmacol Sci. 1993 Dec;14(12):434 – reference: 8081723 - Receptors Channels. 1993;1(2):99-110 – reference: 9362476 - EMBO J. 1997 Nov 17;16(22):6615-25 – reference: 8447425 - Am J Physiol. 1993 Feb;264(2 Pt 1):L116-23 – reference: 8662756 - J Biol Chem. 1996 May 31;271(22):13239-43 – reference: 8964107 - Circulation. 1996 Jul 1;94(1):1-5 – reference: 8279575 - Am J Physiol. 1993 Dec;265(6 Pt 1):L591-7 – reference: 8524851 - Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11796-800 – reference: 8508921 - FEBS Lett. 1993 Jun 14;324(2):205-10 – reference: 7491983 - Am J Physiol. 1995 Nov;269(5 Pt 1):L637-44 – reference: 7517960 - J Clin Pathol. 1994 May;47(5):448-52 – reference: 7788871 - Circ Res. 1995 Jul;77(1):131-9 – reference: 8938716 - Neuropharmacology. 1996;35(7):851-65 – reference: 7615797 - J Clin Invest. 1995 Jul;96(1):282-92 – reference: 7623158 - J Neurosci. 1995 Jul;15(7 Pt 2):5360-71 – reference: 8222081 - Circ Res. 1993 Dec;73(6):1100-12 – reference: 1245025 - Circ Res. 1976 Feb;38(2):99-104 – reference: 8593702 - Circ Res. 1996 Mar;78(3):431-42 – reference: 8204618 - Biochemistry. 1994 Jun 7;33(22):6834-9 – reference: 7977686 - Am J Physiol. 1994 Nov;267(5 Pt 1):C1231-8 – reference: 7473178 - J Pharmacol Exp Ther. 1995 Nov;275(2):864-76 – reference: 8158277 - J Neurosci. 1994 Apr;14(4):2408-17 – reference: 8901674 - Circulation. 1996 Nov 1;94(9):2216-20 – reference: 8304521 - Am J Physiol. 1994 Jan;266(1 Pt 2):H365-70 – reference: 9410914 - J Clin Invest. 1997 Nov 1;100(9):2347-53 |
| SSID | ssj0014454 |
| Score | 2.1229792 |
| Snippet | Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 2319 |
| SubjectTerms | Animals Antibody Specificity Calcium - metabolism Delayed Rectifier Potassium Channels Hypoxia - physiopathology Immunoblotting Immunohistochemistry Kv1.5 Potassium Channel Male Membrane Potentials Mice Muscle, Smooth, Vascular - physiology Potassium Channels - genetics Potassium Channels - physiology Potassium Channels, Voltage-Gated Pulmonary Artery - physiology Rats Rats, Sprague-Dawley Shab Potassium Channels Vasoconstriction |
| Title | Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/9616203 https://www.proquest.com/docview/79923242 |
| Volume | 101 |
| WOSCitedRecordID | wos000074165900004&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3dS9xAEF-sluKL9kvU2nYe-lZTk80mm0BBRCpt7R0-qNzbsZ800EvieR7m_-sf5sxegn0pfehLCIHdTJjJzG92vhj7oKWlpkbolqBzEgnjeVQKm0RO-ywviszx0Ezn-occj4vJpLxYY5-HWhhKqxx0YlDUtjF0Rn4kyzIY_-P2JqKZURRb7QdoPGEbKQIZkmk5eYwhCJH1PZiTqJRp0U8WQot99P30W0qjcv8GKoNxOdv-P7Kes60eVMLJSgpesDVXv2TPRn3Y_BX7PRqG4EJl-_SgwBFoPCACBMoxpHvUVQtUMOHQzcL5R6C64BrN5yGco5-bgarx8ZJ_Sg6hquFn1zb3lYH27hdSouYdLBVymyDnvAoFE2FBnw5PL6BJIGgsYeZm6KbXDtpmQQQh9bgfSuMfe4Vs0w5mXWM6BMSv2dXZl8vTr1E_viEyaPYXEbeIJpWzwupCWJ9oT9hOCxlLnXPhEHgVJhbOCascz1Cz5Nz7xBlUEbFUiu-w9bqp3S4DIV0uVJ6V6N4JY-MydR79SK2NS1OlzR57P3Bnir8HxTzwE5q72-nAnz22s2LwtF118ZiWeZLzON3_59I3bHNViEhHLwdsw6NecG_ZU7NcVLfzd0Ho8Dq-GD0AMUDmcw |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Molecular+identification+of+the+role+of+voltage-gated+K%2B+channels%2C+Kv1.5+and+Kv2.1%2C+in+hypoxic+pulmonary+vasoconstriction+and+control+of+resting+membrane+potential+in+rat+pulmonary+artery+myocytes&rft.jtitle=The+Journal+of+clinical+investigation&rft.au=Archer%2C+S+L&rft.au=Souil%2C+E&rft.au=Dinh-Xuan%2C+A+T&rft.au=Schremmer%2C+B&rft.date=1998-06-01&rft.issn=0021-9738&rft.volume=101&rft.issue=11&rft.spage=2319&rft_id=info:doi/10.1172%2Fjci333&rft_id=info%3Apmid%2F9616203&rft_id=info%3Apmid%2F9616203&rft.externalDocID=9616203 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0021-9738&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0021-9738&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0021-9738&client=summon |